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1
Cruz, Rui Filipe Silva. "Characterization of lipocalin 2 ontogenic expression profile." Master's thesis, Universidade de Aveiro, 2010. http://hdl.handle.net/10773/4009.
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Mestrado em Biologia Molecular e Celular<br>O ferro é essencial para processos metabólicos fundamentais. Dada a sua
natureza reactiva, a homeostasia do ferro é um processo altamente
regulado em mamíferos. Um desequilíbrio no metabolismo do ferro tem
sido associado a patologias como anemia, hemocromatose e doença de
Alzheimer. Ferritina, hepcidina e transferrina são algumas das principais
proteínas envolvidas na manutenção dos níveis de ferro no organismo. A
Lipocalina 2 (LCN2) é uma proteína de 25 kDa pertencente à família das
lipocalinas que tem sido descrita como participante em vários eventos
biológicos, tais como diferenciação do rim, protecção de falha renal,
apoptose, sobrevivência celular e resposta de fase aguda no fígado, baço,
sangue e alguns tecidos epiteliais. Muito relevante é o facto de a LCN2
ser capaz de se ligar a sideróforos bacterianos carregados com ferro.
Durante infecções bacterianas, a LCN2 compete com as bactérias pelo
ferro disponível, limitando assim a proliferação bacteriana. Este efeito
bacteriostático enaltece o papel de LCN2 na resposta imune inata. Dada
a capacidade de LCN2 para se ligar a sideróforos carregados com ferro e
o facto de existirem células que conseguem capturar este complexo, a
LCN2 tem sido proposta como proteína central num putativo mecanismo
de entrega de ferro alternativo ao da transferrina. De maneira a
compreender melhor o papel de LCN2 no metabolismo do ferro bem
como na resposta imune inata, caracterizamos por análise
immunohistoquimica o padrão de expressão da proteína em ratinho, do
desenvolvimento fetal até um ano de idade, em condições
controlo/fisiológicas (injecção com salino) e após estímulo inflamatório
agudo (injecção com LPS). A expressão de LCN2 durante o
desenvolvimento embrionário foi predominante no fígado e rim. O sinal
da proteína persistiu em ambos os órgãos na primeira semana de vida de
animais controlo, sugerindo uma ligação da proteína a processos de
diferenciação e/ou desenvolvimento. No período pós natal, nos animais
injectados com salino a imunoreactividade de LCN2 foi detectada no
baço, timo e rim. A injecção com LPS induziu expressão de LCN2 no
baço, rim, fígado e barreiras do cérebro. Os dados aqui apresentados
indicam que a presença e o perfil de distribuição de LCN2 em alguns
tecidos de ratinho são dependentes da idade e estado fisiológico.<br>Iron is essential for key metabolic mechanisms. Given its reactive nature,
iron homeostasis is a highly regulated process in mammals. Iron
imbalance as been associated to pathologies such as anemia, hemochromatosis and Alzheimer's disease.Ferritin, hepcidin and
transferrin are some of the key proteins involved in the maintenance of
organism iron levels. Lipocalin 2 (LCN2) is a 25 kDa protein from the
lipocalin family that has been reported to participate in a broad range of
biological events, such as kidney differentiation, protection from renal
failure, apoptosis, cell survival and acute phase response in the liver,
spleen, blood cells and some epithelial tissues. Importantly, LCN2 is
capable of binding to bacterial siderophores loaded with iron. During
bacterial infection scenarios, LCN2 competes with bacteria for iron
resources, thus limiting bacterial proliferation. This bacteriostatic effect
highlights the role of LCN2 in the innate immune system response.
Given the ability of LCN2 to bind iron loaded siderophores and the
finding that cells can uptake this complex, LCN2 has been proposed as a
central participant in a putative transferrin-alternative pathway for iron
delivery. In order to further understand the role of LCN2 in iron
metabolism as well in the innate immune system response, we
characterized through immunohistochemical analysis the protein
expression pattern in mice, from fetal development to one year of age,
both in control/physiological conditions (saline injection) and after an
acute inflammatory stimulus (LPS injection). LCN2 expression during
embryonic development was predominant in the liver and kidney. The
protein signal persisted in both organs in the first week of life of control
animals, thus suggesting that the protein may be linked to differentiation
and/or development processes. In control post-natal animals LCN2
immunoreactivity was detected in the spleen, thymus and kidney. LPS
injection induced increased LCN2 expression in the spleen, kidney, liver
and barriers of the brain. The present data indicates that LCN2 presence
and distribution pattern in some mice tissues is dependent of age and
physiological state.
2
Trudel, Nathalie. "Gene expression profile in human prostate cancer cell lines." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=33449.
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Since the beginning of this work in 1998, it is estimated that 1780 men died of prostate cancer in Quebec. Molecular analysis of prostate cancer will eventually lead to the discovery of key genes involved in its onset and progression. The present project was to compare gene expression profiles in human non-tumorigenic versus tumorigenic prostate cell lines generated in our laboratory. A putative tumor suppressor gene present on 12q13 would be responsible for the non-tumorigenic phenotype of one cell line as discovered earlier by our team.<br>In order to compare gene expression patterns, expression arrays from Clontech, bearing 588 genes known to be involved in human cancers, were hybridized with cDNA derived from two related cell lines available in our laboratory. This one experiment provided interesting hints on differentially expressed genes that could be involved in human prostate cancer. Interesting clones were confirmed by Northern blots. When commercial antibody was available, analysis was extended at the protein level. A combination of these analyses revealed no striking difference in the level of expression for the genes previously identified by the arrays hybridization.<br>Simultaneously, differential display PCR techniques, allowing the discovery of unknown differentially expressed molecules and thus complementing the previous approach, were applied to compare related cell lines and unique hybrids. Cloning and sequencing of differential fragments brought us to what could be a new cDNA expressed in many human cell lines.<br>Prostate cancer is not well characterized enough to allow accurate diagnosis or appropriate therapy strategies. Differentially expressed molecules analyzed in this project as well as the putative new cDNA might fulfil part of this lack in the understanding of this disease.
3
Yamaga, Yuichi. "Gene expression profile of Dclk1+ cells in intestinal tumors." Kyoto University, 2019. http://hdl.handle.net/2433/236595.
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4
Feng, Huichen. "Gene expression profile in human trophoblast and gestational trophoblastic disease." Click to view the E-thesis via HKUTO, 2004. http://sunzi.lib.hku.hk/hkuto/record/B31384742.
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Feng, Huichen, and 馮會臣. "Gene expression profile in human trophoblast and gestational trophoblastic disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B31384742.
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Wessagowit, Vasarat. "Keratinocyte gene expression profile in recessive dystrophic epidermolysis bullosa wounds." Thesis, King's College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408868.
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Hohmann, André. "Rights Expression Languages in Libraries : Development of an Application Profile." Thesis, Högskolan i Borås, Akademin för bibliotek, information, pedagogik och IT, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:hb:diva-10693.
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The goal of the thesis is the development of an exemplary application profile for one institution guiding the use of Rights Expression Languages (REL) to include the rights information of digital documents in the metadata. Cultural heritage institutions face many challenges with regard to the growing number of digital documents. One challenge is the effective and efficient management, administration and presentation or publication of the documents according to their inherent rights. A basic issue is the inclusion of the rights information in the metadata file of the digital documents to enable automated administration of the documents. The application profile is supposed to show the REL’s potential for solving the challenge. Whether RELs can be applied practically in the cultural heritage sector is not in the scope of the thesis and must be examined in a large scale study. As applied research, the thesis does not follow a strict quantitative or qualitative research method but gathers, examines and evaluates data to develop an application profile. Due to the focus on technical issues, it aims at developers and not at end users. To reach the thesis’ goal, RELs are located in the area of digital rights. Four RELs are examined basi-cally by literature analysis. In addition, various representative licenses from one library are chosen which are “translated” into the most appro-priate REL. The findings flow into a prototype application profile which is evaluated in one iteration step by experts according to heuristic evaluation to identify technical and conceptual flaws. Based on the identified flaws, the prototype is revised. Finally, the exemplary application profile for the METS metadata schema is presented and recommendations for further elaborated appli-cation profiles are given.
8
Ferreira, Violeta Silva. "MicroRNA expression profile of Danio rerio brain exposed to ethanol." Master's thesis, Universidade de Aveiro, 2010. http://hdl.handle.net/10773/8982.
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Mestrado em Biologia Molecular e Celular<br>miRNAs are short (~22 nt) non-coding RNA molecules that control gene
expression at post-transcription level by degrading or inhibiting particular target
genes. miRNAs are abundant in vertebrate genomes where they play an
important role on the control of cell proliferation and differentiation, apoptosis,
neurogenesis and synaptic plasticity. Although legally commercialize, alcohol is
toxic for living organisms and its consumption can induce dependence. The
regular alcohol intake increases the risk of hepatic disease and certain cancers,
having a deleterious effect on the immune, endocrine and nervous system. The
brain is not only an important target for alcohol metabolites, but also a rich
source of miRNAs. Using miRNA microarrays approach, we aimed to
understand how chronic (0.25% EtOH) and acute (0.25%; 0.5%, 1 e 1.5%
EtOH) ethanol exposure affects miRNA expression.
The results demonstrate that chronic ethanol intake deregulated the expression
of 32 miRNAs. From those, miR-9, miR-23a, miR-30e, miR-133a, miR-181
were over-expressed and miR-16a, miR-145 and miR-181b were inhibited. The
putative target genes for those miRNAs are implicated in cell cycle,
differentiation, apoptosis and cell adhesion. The acute ethanol exposure also
deregulated miRNA expression profile and each ethanol concentration shows a
distinct miRNA expression profile. For example, the pro-apoptotic miRNA miR-
23a is up-regulated in chronic ethanol exposure but is down-regulated in the
higher ethanol concentrations (1 e 1.5% EtOH) of acute test. These results
suggest that alcohol consumption, even consumed in a short-period or
concentration, affects the expression of miRNAs. Possibly, these alterations
have implications on cellular cycle and apoptosis and therefore they could
contribute to a higher risk of developing tumours.<br>Os miRNAs são pequenas moléculas (~22 nt) de RNA não-codificante que
regulam a expressão genética ao nível pós-transcripcional através da
degradação ou inibição dos genes alvo. Os miRNAs são abundantes nos
genomas eucariótas, onde desempenham funções importantes no controlo da
proliferação e diferenciação celular, apoptose, neurogénese e plasticidade
sináptica. Apesar de ser uma substância legal, o álcool é tóxico para os seres
vivos e o seu consumo regular pode induzir dependência. O consumo
excessivo de álcool aumenta o risco de doença hepática e de determinados
cancros e tem efeitos deletérios ao nível do sistema imunitário, endócrino e
nervoso. O cérebro, para além de ser um importante alvo dos metabolitos do
álcool, é um dos órgãos com maior expressão de miRNAs. Através da análise
de microarrays de miRNAs pretendeu-se entender de que modo a exposição
crónica ao etanol (0.25% EtOH) e a exposição aguda a um pulso de etanol
(0.25%; 0.5%, 1 e 1.5% EtOH) afectam a expressão dos miRNAs. A expressão
de 32 miRNAs foi significativamente alterada pela exposição crónica ao etanol,
destacando-se o aumento da expressão do miR-9, miR-23a, miR-30e, miR-
133a, miR-181 e a diminuição na expressão do miR-16a, miR-145 e miR-181b.
Genes envolvidos no ciclo celular, diferenciação, apoptose e adesão celular
parecem ser os alvos preferenciais destes miRNAs. A exposição aguda
também alterou a expressão de vários miRNAs, que variam consoante a
concentração de etanol utilizada. Por exemplo, a expressão do miRNA próapoptótico
miR-23a aumentou durante a exposição crónica ao etanol e
diminuiu com o aumento da concentração do tóxico (1 e 1.5% EtOH) durante o
teste agudo. Estes resultados sugerem que o consumo de álcool, mesmo num
curto espaço de tempo ou concentração, afecta a expressão dos miRNAs.
Possivelmente essas alterações têm implicações no ciclo celular e apotose,
podendo contribuir deste modo para um risco acrescido de desenvolver
tumores.
9
Rashid, Susan Basel. "Protein Profile and Directed Gene Expression of Developing C2C12 cells." Youngstown State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ysu1442433668.
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10
Malmberg, Jennie. "The neuroanatomical expression profile of novel membrane proteins. : The effect of macronutrients on gene expression." Thesis, Mälardalen University, School of Sustainable Development of Society and Technology, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:mdh:diva-1105.
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<p>Worldwide obesity is an increasing problem. Apart from the fact that obesity greatly impairs the health, quality and length of life for the affected individuals, it is also has the potential to become a major socioeconomic problem in a near future. However preventive actions require an understanding of the cause. Before the psychological influence on eating can be evaluated a profound understanding of the biological regulatory system and how this interacts with the food consumed is required. On the assumption that food consumption is regulated by interplay between food and genes, the food itself may influence the genes that regulate consumption, hence change the expression levels of the genes regulating food intake. To evaluate the interplay between food and gene expression, the project contained several parts, reflecting different aspects of the area of research. The feeding studies had in common that they were initial trials in a larger project. The results of these will be evaluated and used in combination with further studies. The mice typed for food preference illustrate the complexity of the feeding regulatory system by pointing out the differences between individuals even in a relatively small group of animals. Mice in general like food high in fat and here the animals that showed a preference for sugar also showed a significant increase in their intake of chow. Since chow consists mainly of carbohydrates the results might indicate a preference not for sucrose in particular but for carbohydrates in general. The effect this may have on other studies is still unclear as further studies are needed to determine whether the difference may be the result of an innate genetic difference. Leucine has been previously shown to reduce the total caloric intake. When given in combination with palatable food the addition of Leucine primarily reduced the intake of chow. From a dietary perspective this would translate to a preference to sweets and fast food at the expense of food with more nutritious content. The RT-PCR analysis’s gives clues to how the energy regulatory circuitry responds to the intake of selected macronutrients. When it comes to gene expression there is a significant effect of macronutrients on the gene expression levels. The common theme for many of the genes tested seems to be down regulation of satiety signals, as if to support over feeding on palatable diets and in many cases sucrose in particular. The intake of macronutrients such as sugar or fat has been showed to have an effect on the feeding regulatory circuitry, demonstrated by the change in gene expression levels. The response to said macronutrients is site specific which is clearly shown both by RTPCR analysis of samples from different parts of the brain, such as the brainstem or hypothalamus, and by immunohistochemistry of selected areas. The immunohistochemistry also confirms that the novel Oxytocin receptor-antagonist, who is injected IP, actually passes over the blood-brain barrier and has an actual affect on the regions of interest. The areas affected by the antagonist can be visualized and identified through the staining of active sites.</p>
11
Dhawan, Manik. "Application of Committee k-NN Classifiers for Gene Expression Profile Classification." University of Akron / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=akron1227547457.
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Sprissler, Ryan S., Jacy L. Wagnon, Rosie K. Bunton-Stasyshyn, Miriam H. Meisler, and Michael F. Hammer. "Altered gene expression profile in a mouse model of SCN8A encephalopathy." ACADEMIC PRESS INC ELSEVIER SCIENCE, 2017. http://hdl.handle.net/10150/622816.
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12 month embargo; Available online 9 November 2016<br>SCN8A encephalopathy is a severe, early-onset epilepsy disorder resulting from de novo gain-of-function mutations in the voltage-gated sodium channel Na(v)1.6. To identify the effects of this disorder on mRNA expression, RNA-seq was performed on brain tissue from a knock-in mouse expressing the patient mutation p.Asn1768Asp (N1768D). RNA was isolated from forebrain, cerebellum, and brainstem both before and after seizure onset, and from age-matched wildtype littermates. Altered transcript profiles were observed only in forebrain and only after seizures. The abundance of 50 transcripts increased more than 3-fold and 15 transcripts decreased more than 3 fold after seizures. The elevated transcripts included two anti-convulsant neuropeptides and more than a dozen genes involved in reactive astrocytosis and response to neuronal damage. There was no change in the level of transcripts encoding other voltage-gated sodium, potassium or calcium channels. Reactive astrocytosis was observed in the hippocampus of mutant mice after seizures. There is considerable overlap between the genes affected in this genetic model of epilepsy and those altered by chemically induced seizures, traumatic brain injury, ischemia, and inflammation. The data support the view that gain-of-function mutations of SCN8A lead to pathogenic alterations in brain function contributing to encephalopathy.
13
Johnson, Eric Eugene. "A profile of the expression of a metabolic gene cluster in Arabidopsis." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/42802.
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Plant cells often display a microtubule reorganization event when encountered with stress. This has been found to be integral for the reaction to stresses such as aluminum toxicity and cold stress. A cDNA microarray was previously conducted that identified MARNERAL SYNTHASE (MRN1), an oxidosqualene cyclase that produces the triterpene marneral, as the most highly upregulated gene when microtubule dynamics are disrupted in Arabidopsis. This work identifies two cytochrome P450s, CYP71A16 and CYP705A12, that are highly coregulated with MRN1 and are located within close proximity to the MRN1 loci. Using GC-FID and GC-MS, MRN1 and CYP71A16 are shown to function together in a single pathway in what is known as a metabolic gene cluster, while further testing shows that they are not in fact regulated by microtubule dynamics.
The expression profile of these genes is explored since there is no known function for marneral or its related metabolites. Using a promoter-reporter and real time PCR analysis, it was found that the hormones ABA and methyl jasmonate induce expression of the three genes to different degrees depending on seedling age. Osmotic stressors, including mannitol and NaCl treatments, also induce the expression of these genes. MRN1, in particular, seems to show the highest level of induction suggesting that the pathway is transcriptionally regulated through MRN1. These conditions are shown to not affect the growth response in mutant plants unable to metabolize marneral or plants ectopically expressing different combinations of the three genes.
These conditions are intriguing because most triterpenes derived from secondary metabolism are generally thought to play roles in defense, yet these data suggest that the pathway is induced under abiotic stress conditions. The marneral cluster may have evolved to be expressed under osmotic stress conditions in a sense to protect the plants water from pathogens or herbivores. It is also reasonable to speculate that these compounds may play roles in signalling or membrane modification. Further experiments are proposed that could test these hypotheses.
14
Ng, Tsz Lui Michelle. "Characterizing the expression profile of angiogenic proteins after acute spinal cord injury." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/42577.
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Spinal cord injuries (SCI) are one of the most physically and psychologically devastating injuries one can survive. Despite decades of intense research effort, robust therapeutic treatment for this catastrophic condition remains elusive. The nature of the sequelae of SCI is characterized by progressive cell death in the injury penumbra, resulting in further neurological impairments. The intricate relationship between the vascular and nervous systems has become increasingly evident in many aspects of both normal physiology, and various pathological conditions, including SCI. Vascular abnormalities play a central role in the propagation of secondary damage after SCI.
The aim of this thesis is to further the understanding of the vascular changes that occur after acute SCI. The endogenous expression of three angiogenic proteins: Angiopoietin-1 (Ang1), Angiopoietin-2 (Ang2) and Angiogenin will be examined after acute traumatic SCI. In the first study, the concentration of these proteins will be measured in a temporal series of cerebrospinal fluid (CSF) samples after human SCI. In the second study, the relative protein expression of Ang1 and Ang2 will be characterized in rat spinal cord after SCI.
In human, Ang1 in CSF is not significantly different from non-SCI values after the initial spike at 24 hours post-SCI. Ang2 in CSF shows a delayed but persistent increase through the first 5 days post-SCI. In contrast, Ang1 in rat spinal cord decreases as early as 2 hours post-SCI, while low molecular weight Ang2 increases dramatically after SCI, from 2 hours to 3 days post-injury, peaking with a 13-fold elevation at 24 hours post-injury. These findings represent the first description of these proteins in the acute SCI setting in human CSF and rat spinal cord. The sustained elevation of Ang2 illustrates a possible mechanism by which reported vascular dysfunction and increases in blood-spinal cord-barrier (BSCB) permeability occurs after SCI. The patterns of change reported between the two studies may allude to the feasibility of using CSF as a biological proxy to future investigations into the biochemical events which occur in the spinal cord after SCI, and guide the development of pharmacologic treatments for this devastating condition.
15
Ouyang, Ping. "Effect of exercise-induced weight control on phospholipid profile and gene expression." Diss., Manhattan, Kan. : Kansas State University, 2007. http://hdl.handle.net/2097/519.
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Jiang, Pingping, and 姜平平. "Differential protein expression profile in intestine of preterm piglets with necrotizing enterocolitis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B41633866.
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Di, Palo Benedetta <1984>. "Streptococcus agalactiae adapts to glucose stress conditions by modulating gene expression profile." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2012. http://amsdottorato.unibo.it/4805/.
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Diabetes mellitus is considered a risk factor for Group B Streptococcus (GBS) infections. Typically, this pathology is associated to high glucose levels in the bloodstream. Although clinical evidences support this notion, the physiological mechanisms underlying GBS adaptation to such conditions are not yet defined. In the attempt to address this issue, we performed comparative global gene expression analysis of GBS grown under glucose-stress conditions and observed that a number of metabolic and virulence genes was differentially regulated. Of importance, we also demonstrated that by knocking-out the csrRS locus the transcription profile of GBS grown in high-glucose conditions was profoundly affected, with more than a third of glucose-dependent genes, including the virulence factor bibA, found to be controlled by this two-component system. Furthermore, in vitro molecular analysis showed that CsrR specifically binds to the bibA promoter and the phosphorilation increases the affinity of the regulator to this promoter region. Moreover, we demonstrated that CsrR acts as a repressor of bibA expression by binding to its promoter in vivo. In conclusion, this work by elucidating both the response of GBS to pathological glucose conditions and the underlined molecular mechanisms will set the basis for a better understanding of GBS pathogenesis.
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Jiang, Pingping. "Differential protein expression profile in intestine of preterm piglets with necrotizing enterocolitis." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B41633866.
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Yin, Yalei. "Analysis of transgene expression profile-dependent induction of transgene-specific immune response." 京都大学 (Kyoto University), 2014. http://hdl.handle.net/2433/192152.
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Wright, Rachael Deborah. "Modulation of galectin expression and glycosylation profile of immune cells during inflammation." Thesis, Queen Mary, University of London, 2015. http://qmro.qmul.ac.uk/xmlui/handle/123456789/9014.
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Galectins-1, -3 and -9, are endowed with many immune-regulatory properties, with galectins-1 and -9 largely regarded as anti-inflammatory and galectin-3 as pro-inflammatory. Expression levels increase in activated adaptive immune cells, with peak expression often correlating with peak inflammation. Galectin actions are not only determined by their expression levels but also target tissue permissibility to galectin binding, which is in turn determined by the profile of specific carbohydrate residues, namely N-acetyllactosamine, recognised by these lectins. How expression levels and actions are modulated in innate immune cells during inflammation has not been systematically characterised. This study therefore set out to delineate the effects of inflammation on neutrophil glycophenotype, as well as elucidate the temporal and spatial modulation of galectins during resolving inflammation. The neutrophil glycophenotype was modulated during trafficking with decreased levels of all terminal glycan residues assessed. However, this did not correlate with galectin binding permissibility suggesting this is not a useful indicator in this model. The overall change in glycosylation may theoretically be a consequence of rapid modulation of cell surface glycoproteins by activated neutrophils (i.e. CD62L shedding) rather than the actions of specific glycosylation enzymes as demonstrated in T- and endothelial cells. Assessment of galectin levels in leukocytes over a 96h zymosan-induced resolving peritonitis demonstrated alterations both spatially and temporally with increased galectin-3 expression in neutrophils at the inflammatory site compared to the periphery and a peak expression at 24h adding supporting evidence that modulation of galectin expression allows delineation of galectin responses by neutrophils. This study also demonstrated a novel pro-resolution effect of galectin-3 with defective resolution observed in galectin-3 null mice. In conclusion this work demonstrated that neutrophil permissibility for galectins-1, -3 and -9 binding is more likely a consequence of the exposure to galectins at specific time points in the resolving inflammatory response rather than due to a modulation of the glycophenotype upon activation. This study also 3 demonstrated that as well as an important role in the induction of an inflammatory response galectin-3 is involved in resolution, a novel finding which may lead to a better understanding of the resolution process.
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Kaur, Sukhbir. "Characterisation of the expression profile and endothelial function of Rho GTPase RhoJ." Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/1558/.
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Rho GTPases are molecular switches that regulate many aspects of cell physiology. A number of Rho GTPases are essential for the formation of new vessels from pre-existing ones, a process known as angiogenesis. RhoJ/TCL belongs to the Cdc42 subfamily of Rho GTPases. Previous bioinformatic and primary cell line analyses identified RhoJ as being highly expressed in endothelial cells. The aim of this project was to investigate the expression pattern and endothelial function of RhoJ, particularly in the processes necessary for angiogenesis. Silencing RhoJ with siRNA impaired tube formation and migration. On the cellular level, RhoJ knockdown increased focal adhesions, actin stress fibres and collagen gel contraction, suggesting increased actomyosin contractility. Pharmacological inhibition of ROCK and myosin II, two regulators of actomyosin contractility, restored motility and tube formation after RhoJ knockdown. RhoJ localised to blood vessels of developing mice and in various human normal and pathological tissues. In zebrafish embryos RhoJ was not expressed in endothelial cells, instead RhoJ was expressed in the musculature where it was involved in regulating somite formation. This study is the first to describe a role for RhoJ as a negative regulator of focal adhesion numbers and actomyosin contractility and to demonstrate a critical role of this Rho GTPase in endothelial cell migration and tube formation, thus identifying a potential new player in angiogenesis.
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Bing, Nan. "Statistical Analysis of Gene Expression Profile: Transcription Network Inference and Sample Classification." Diss., Virginia Tech, 2004. http://hdl.handle.net/10919/11139.
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The copious information generated from transcriptomes gives us an opportunity to learn biological processes as integrated systems; however, due to numerous sources of variation, high dimensions of data structure, various levels of data quality, and different formats of the inputs, dissecting and interpreting such data presents daunting challenges to scientists. The goal of this research is to provide improved and new statistical tools for analyzing transcriptomes data to identify gene expression patterns for classifying samples, to discover regulatory gene networks using natural genetic perturbations, to develop statistical methods for model fitting and comparison of biochemical networks, and eventually to advance our capability to understand the principles of biological processes at the system level.<br>Ph. D.
23
Kamran, Maryam. "Expression Profile of flbD During Morphogenesis in the Dimorphic Fungus Penicillium Marneffei." Youngstown State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ysu1329770446.
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Ballis, Andreas. "Gene expression profile of cells in successive stages of corneal stem cell lineage." Thesis, Cardiff University, 2006. http://orca.cf.ac.uk/56073/.
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In this study the complete transcriptome of groups of cells at specific successive stages of the complete corneal stem cell hierarchy was revealed. The cornea presents a linear differential distribution of each type of cell of this hierarchy, with stem cells, transient amplifying cells and mature cells residing predominantly in the basal limbal, peripheral and central corneal epithelium respectively. In order to realise the complete set of genes that are up or down regulated at each stage of the corneal stem cell lineage, a Laser Micro-dissection and pressure Catapulting method was optimised, that allows for isolation of the desired type of cell from the specific areas they predominate, in a manner that would not challenge the integrity of their mRNA, as determined by 3'-5' relative ratios, estimated by semi-quantitative RT-PCR. To analyse the relative abundance of every gene in each of the cell types that were isolated, a linear amplification of mRNA method had to be optimised, as determined by comparing the relative abundances of specific endogenous and exogenous gene transcripts before and after the amplification reaction, using high density oligonucleotide arrays. In order to amplify the mRNA in such a manner and to such a degree that it could be analysed by high density oligonucleotide arrays an in-vitro transcription based amplification method was employed and optimised. The method entailed the generation of double stranded cDNA reverse transcripts carrying the T7 RNA polymerase promoter and subsequent in-vitro transcription that yielded large amounts of linearly amplified mRNA (aRNA) The midfield of data that was produced was analysed by appropriate mathematical methods such as Robust Multiarray Analysis and in order to obtain a set of genes that are up or down regulated specifically in each cell type. Principal Component analysis confirmed the validity of the hypothesis that the variance in gene expression arose from the fact that different types of cells were analysed The results were validated by semi-quantitative RT-PCR analysis, which confirmed the sensitivity of the arrays. Additionally several protein targets that were indicated by the array analysis were studied by immunohistochemical methods. The putative differential mechanisms regulating corneal epithelial stem and well as transient amplifying cell fate and corneal homeostasis are discussed. The results of this study are likely to augment the efforts of understanding corneal epithelial stem cells and possibly other adult stem cells and thereby assist in future research and therapeutic interventions involving stem cells.
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Ranghini, Egon Jacopo. "Evaluating the expression profile and developmental potential of mouse kidney-derived stem cells." Thesis, University of Liverpool, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.539593.
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Matsusaki, Takashi. "Gene expression profile of macrophage-like U937 cells in response to polyethylene particles." Kyoto University, 2008. http://hdl.handle.net/2433/135865.
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Lu, Chen. "Expression profile of multidrug resistance genes and proteins in cancerous and stem cells." Thesis, University of Central Lancashire, 2008. http://clok.uclan.ac.uk/19754/.
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Despite improved knowledge and advanced treatments of high-grade gliomas, the overall survival rate of glioma patients remains low due to the recurrences and locations of the tumour. Evidence shows that the existence of a subpopulation of cells - cancer stem cells (CSCs) may be the major obstacle in treating gliomas. CD133 and nestin have been suggested as the markers of CSCs and natural stem cells. The primary focus of this study was to identify CD133+/nestin+ stem-like cells and discover their association with multidrug resistance (MDR) related genes, i.e. multiple drug resistance I (mdrl) gene and anti-apoptotic gene (bcl-2) in human glioma compared to normal brain tissues and cell lines. Glioma and normal astrocyte cell lines have been employed for CD133 isolating purposes to characterise the association with MDR related genotype and phenotype. The chemosensitivity of the isolated CD 133 population was investigated using chemosensitivity assay. Meanwhile, a serum deprivation method was established in this study to enrich and select CD 133+ CSCs in a glioma (GOS-3) cell line. As a secondary focus of this project, the possibility of immortalisation enzyme hTERT being a discriminative masker between normal and cancer brain stem cells and the transcriptional correlation between cd133 and bmi-lIc-myc oncogenes were investigated. For the first time, findings of the current study demonstrated that 1) there was an evident increase of CD133 gene expression in glioma compared to normal brain tissues where the latter expressed low levels of CD133, P-gp and Bcl-2 than glioma tissues, with an exception of nestin expression, 2) serum deprivation enriched CD133 expression and demonstrated a direct coexpression between CD133 and drug resistance in GOS-3 cells, 3) hTERT may not be a discriminative marker for normal and cancer brain stem cells, 4) although there was a strong transcriptional association between bmil and cmyc, there was an inverse transcriptional association between these genes and cd133 in serum deprived glioma cells, suggesting that bmil may not be essential for the maintenance of glioma stem cells, and 5) CD133+ glioma and normal brain cells showed a significantly high resistance towards chemotherapeutic drugs compared to the autologous CD133- cells. In conclusion, an improved understanding of molecules contributing to the maintenance of CSCs may lead to a combined treatment, targeting both CSCs and their protective MDR phenotypes leading eventually to attractive strategies for the treatment of gliomas.
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Middleton, Rachel Katharine. "An investigation into the cytokine expression profile of the abdominal aortic aneurysm wall." Thesis, University of Leicester, 2006. http://hdl.handle.net/2381/29890.
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Abdominal aortic aneurysm is a disease commonly found in elderly males involving dilatation of the abdominal aorta. The aneurysm wall is characterised by a decrease in the elastin/collagen ratio, apoptosis of smooth muscle cells and a prominent inflammatory infiltrate. Degradation of the extracellular matrix has been attributed to matrix metalloproteinases (MMP), the expression and activation of which is tightly regulated by inflammatory mediators such as cytokines. The presence of an inflammatory infiltrate is a potential source of cytokines within the aneurysm wall.;The aim of this thesis is to investigate the nature of the cytokines that are expressed within the aneurysm. Further work aims to characterise the expression of key cytokines and to investigate their effect on MMP expression.;The cytokine profile of the aneurysm wall was measured using a 42-cytokine protein array. Overall, a number of pro-inflammatory cytokines, chemokines and growth factors were raised within the aneurysm wall. Interleukin-6 (IL-), IL-8, monocyte chemoattractant protein-1 (MCP-) and MCP-2 were highly elevated in the aneurysm above the physiological levels found in abdominal and thoracic aorta.;The expression of chemokines within the aneurysm wall was characterised further using immunohistochemistry. IL-8 was found to co-localise with the infiltrate, which was predominantly formed from CD20+ B-lymphocytes and CD3+ T-lymphocytes, whilst MCP-1 co-localised to CD68+ macrophages.;The effect of IL-8 on the expression of MMP-2 and MMP-9 was investigated through an in vitro aneurysm model. The results showed that MMP-2 was expressed constitutively, whilst MMP-9 expression from the same culture decreased with time. IL-8 did not effect MMP-2 and MMP-9 expression.;In conclusion, the abdominal aortic aneurysm wall is a highly pro-inflammatory and chemotactic environment. Co-localisation of IL-8 and MCP-1 with the infiltrating cells suggests a role for these cytokines in aneurysm pathogenesis. However, a direct involvement between IL-8 and MMP expression is unlikely.
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Calyjur, Priscila Clara. "Efeitos da mutação mdx no background 129/Sv." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/41/41131/tde-17072015-142001/.
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O camundongo mdx, modelo murino para a Distrofia Muscular de Duchenne (DMD) possui uma mutação de ponto no gene da distrofina que resulta na ausência da proteína no músculo, porém seu fenótipo é brando o que o torna um bom modelo genético e molecular, mas não um bom modelo funcional. Esperando obter um modelo para DMD que tivesse um fenótipo mais fiel ao apresentado pelos pacientes humanos, optou-se por transferir a mutação mdx para o background 129/Sv. Através de cruzamentos sucessivos foram obtidas 3 gerações de animais mdx com background 129/Sv (mdx129) e cada geração foi avaliada funcionalmente por 6 meses. Desde a primeira geração é possível observar que os animais mdx129 são mais fortes do que os mdx originais em background C57BL (mdxC57BL), sendo o oposto do esperado no início dos experimentos. O estudo então foi redirecionado para tentar entender o motivo dessa melhora. Em relação ao padrão histológico, em geral há diferenças entre o mdxC57BL e mdx129. Observa-se também que os animais mdx129 entram no processo de degeneração mais tardiamente que os animais mdxC57BL e seu processo de regeneração se estende por mais tempo. Através de estudos de microarray foi possível observar que os animais 129/Sv apresentam poucos genes diferencialmente expressos (GDEs) em relação aos animais C57BL, portanto os dois backgrounds são muito semelhantes. O mdxC57BL apresenta muito mais GDEs em relação ao seu selvagem (C57BL) do que o mdx129 em relação ao 129/Sv, entretanto, ambos os modelos apresentam mais genes superexpressos do que subexpressos, indicando que as alterações distróficas e regenerativas estão mais associadas com a ativação do que a repressão de genes. Quando os GDEs de ambos os modelos de mdx são distribuídos em categorias funcionais, há o predomínio de genes ligados ao sistema imune e quando essa categoria é omitida para melhor visualização das restantes, observa se que ambos os modelos apresentam categorias funcionais semelhantes, porém com proporções diferentes. No modelo mdx129 se destaca a diminuição da participação da categoria de rota endo/exocítica (tráfego de vesículas) e homeostase e aumento da participação das categorias de matiz extracelular e atividade enzimática. Cada modelo apresenta genes exclusivos, destacando os genes SPP1 e IL1RN na comparação 129/Sv x mdx129F3. O gene SPP1 codifica a proteína osteopontina (OPN) e o polimorfismo rs28357094 neste gene é utilizado como biomarcador de prognóstico para DMD. O papel da OPN na progressão da distrofia não é bem conhecido. Alguns estudos afirmam que a ausência dessa proteína melhora a força muscular de camundongos mdx, enquanto outros apontam que sua participação é necessária para a regeneração muscular. Assim sendo, mais estudos serão necessários para verificar qual seria a via responsável pela melhora fenotípica do modelo mdx129. Já o gene IL1RN codifica a proteína IL-1Ra, a qual é um antagonista de interleucina 1 (citocina pró-inflamatória e pró fibrótica). Portanto o aumento da expressão do gene de seu antagonista sugere que os animais mdx129F3 podem estar mais protegidos do processo inflamatório causado por essas moléculas. Quando analisadas as listas filtradas para músculo esquelético das comparações C57BL x mdxC57BL e 129/Sv x mdx129F3 para a formação de vias metabólicas, foi gerada apenas uma via em ambas as comparações com número relevante de moléculas. A via gerada pela análise da lista C57BL x mdxC57BL possui mais moléculas do que a via gerada pela analise da lista 129/Sv x mdx129F3, porém, todas as moléculas presentes nesta via, estão presentes na via C57BL x mdxC57BL, indicando que mesmo com número diferente de moléculas envolvidas, os genes participam das mesmas vias. Tanto a comparação de cada geração de mdx129 com o 129/Sv como a comparação das gerações entre si mostram que os efeitos da mudança de background estão presentes desde a primeira geração e não se alteram significativamente com os cruzamentos sucessivos.<br>The mdx mouse, murine model for Duchenne Muscular Dystrophy (DMD) has a point mutation in the dystrophin gene that results in the absence of the protein in the muscle, however its phenotype is mild, which makes it a good genetic and molecular model, but not a good functional model. Hoping to obtain a model for DMD with a phenotype that is more similar the patients\', it was chosen to transfer the mdx mutation to the 129/Sv background. Through successive breedings, 3 generations of mdx animals with 129/Sv background were obtained and each generation was functionally evaluated for 6 months. Since the first generation it is possible to observe that the mdx129 animals are stronger than the original mdx with C57BL background. The results were the opposite of what was expected in the beginning of the experiments, therefore the study was redirectioned to try to understand the reason of the improved phenotype. About the general histological pattern, there are differences between mdxC57BL and mdx129. It can be observed that the mdx129 animals enter the degenerative process later than the mdxC57BL animals and the regenerative process lasts longer. Through microarray studies it was possible to observe that the 129/Sv animals present few differentially expressed genes (DEGs) in comparison to the C57BL animals; therefore both backgrounds are very similar. The mdxC57BL presents many more DEGs in comparison to C57BL than mdx129 in comparison to 129/Sv, however both models present more super expressed genes than sub expressed, indicating that the dystrophic and regenerative alterations are more associated to the activation rather than the repression of genes. When the DEGs of both mdx models are distributed in functional categories, there is the predominance of genes related to the immune system and when this category is omitted for the better visualization of the remaining, it can be observed that both models present similar functional categories, but with different proportions. In the mdx129 model we can highlight the decrease in participation of the endo/exocytic pathway (vesicle traffic) and homeostasis categories, and increase in participation of the extracellular matrix and enzymatic activity categories. Each model presents exclusive genes, highlighting SPP1 and IL1RN in the comparison 129/Sv x mdx129F3. SPP1 encodes the protein osteopontina (OPN) and the polymorphism rs28357094 in this gene is used as a DMD prognostic biomarker. The role of OPN in the dystrophy progression is not well known. Some studies claim that the absence of OPN increases the muscle strength of the mdx mouse, while others indicate that its participation is necessary to muscle regeneration. More studies are needed to ascertain what pathway is responsible for the phenotypic improvement of the mdx129 model. The IL1RN gene encodes the protein IL-1Ra, and interleukin 1 antagonist, which is a pro-inflammatory and pro-fibrotic cytokine. Therefore, the increase in the expression of its antagonist suggests that the mdx129F3 animals may be more protected from the inflammatory process caused by these molecules. When the filtered lists for skeletal muscle of the comparisons C57BL x mdxC57BL e 129/Sv x mdx129F3 were analyzed for the formation of metabolic pathways, only one pathway was generated in both comparisons. The pathway generated in the analysis C57BL x mdxC57BL has more molecules that the one generated by the 129/Sv x mdx129F3 list, but all molecules present in the latter are also present in the former, indicating that even with different numbers of molecules involved, the genes participate in the same pathways. The comparisons of each generation of mdx129 with the 129/Sv and the comparison of the generations among each other show that the effects of the background change are present since the first generation and are not altered with the successive breedings.
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Du, Plessis Juanelle. "Deciphering the impact of rpoB mutations on the gene expression profile of Mycobacterium tuberculosis." Thesis, Stellenbosch : Stellenbosch University, 2014. http://hdl.handle.net/10019.1/86755.
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Thesis (MScMedSc)--Stellenbosch University, 2014.<br>ENGLISH ABSTRACT: Mycobacterium tuberculosis is the etiological agent for tuberculosis, an infectious disease which is one of the leading causes of morbidity and mortality in developing countries. The emergence of drug resistant tuberculosis has negatively impacted the efficacy of current treatment regimens and threatens to undermine tuberculosis control programs worldwide. Rifampicin forms the backbone of the World Health Organization’s recommended treatment regimen for the treatment of drug susceptible tuberculosis. Resistance to rifampicin is caused by mutations in the 81 bp core region of the rpoB gene which encodes the β subunit of RNA polymerase. Numerous studies have shown that mutations at codons 531 and 526 are the most frequent in clinical isolates, yet little is known concerning the mechanistic effect of these mutations on the fidelity of RNA polymerase. In the present study, we aimed to determine the influence of rpoB mutations on the gene expression profile of M. tuberculosis cultured in vitro. To accomplish this, rifampicin resistant clinical isolates and spontaneous mutants (selected in vitro from H37Rv and a drug-sensitive clinical strain) harbouring rpoB H526Y and S531L mutations were subjected to whole genome sequencing and genome-wide transcriptional profiling. When comparing the transcription profile of H37Rv to the in vitro rpoB mutants, a large proportion of the differentially expressed genes were found to encode for proteins involved in intermediary metabolism and respiration; and cell wall and cell processes. The majority of these differentially expressed genes were downregulated. Prominent differential expression in the same functional categories was also evident when comparing the clinical isolates with these mutations; however, a greater number of genes were differentially expressed in this case. Furthermore, expression of genes that are part of the WhiB7 regulon were found to be upregulated in the rpoB526 mutants, and downregulated in the rpoB531 mutants. These findings indicate that both the position of the rpoB mutation, as well as the genetic background of the strain, play an important role in the gene expression profile of rpoB mutants. Surprisingly, transcriptional profiling of cultures that were exposed to the critical concentration of rifampicin for 24 hours did not exhibit significant differential gene expression. Whole genome sequencing, followed by bioinformatic analysis, revealed that the in vitro mutants harbour synonymous and non-synonymous single nucleotide polymorphisms in addition to the respective rpoB mutations. This suggests that the mycobacterial genome is constantly evolving, challenging previous assumptions of relatively static mycobacterial genomes.
The findings from this research have provided novel insight into understanding the influence of resistance-conferring mutations on the biology of M. tuberculosis and have shown that further studies are urgently needed to better understand the complex physiology of this pathogen. This knowledge will be critical for the success of future drug development endeavours.<br>AFRIKAANSE OPSOMMING: Mycobacterium tuberculosis is die etiologiese agent vir tuberkulose, een van die grootste oorsake van morbiditeit en sterftes in ontwikkelende lande. Die verskyning van middelweerstandige tuberkulose het 'n negatiewe impak op die effektiwiteit van die huidige behandeling van tuberkulose en dreig om tuberkulose beheerprogramme wêreldwyd te ondermyn. Weerstandigheid teen rifampisien, een van die eerste-lyn anti-tuberkulose middels, word veroorsaak deur mutasies in die 81 bp kerngedeelte van die rpoB geen. Die mees algemene mutasies in kliniese isolate word gevind in kodons 531 en 526; alhoewel daar min inligting beskikbaar is oor die effek van hierdie mutasies op die funksie van RNS polimerase. Die doel van hierdie studie was om die effek van verskillende rpoB mutasies op die geen-uitdrukkingsprofiel van M. tuberculosis te bepaal. Rifampisien-weerstandige kliniese isolate en in vitro mutante (geselekteer vanaf H37Rv en 'n rifampisien-sensitiewe kliniese isolaat) met rpoB H526Y en S531L mutasies was vir hierdie doel geselekteer en gebruik om die heel genoom volgorde te bepaal en geenuitdrukking te kwantifiseer. Vergelyking van die H37Rv transkripsieprofiel met in vitro geselekteerde rpoB mutante het getoon dat 'n groot aantal gene wat differensieel uitgedruk is, vir proteïene kodeer wat betrokke is in selwand-prosesse en intermediêre metabolisme en respirasie. Die meerderheid van hierdie differensieel uitgedrukte gene was afgereguleer. ’n Soortgelyke verskynsel is ook waargeneem in kliniese isolate, met die verskil dat 'n groter aantal gene in hierdie geval differensieel-uitgedruk was. Gene wat deel vorm van die WhiB7 regulon is opgereguleer in die rpoB526 mutante, terwyl dit afgereguleer was in die rpoB531 mutante. Hierdie resultate is ’n baie sterk aanduiding dat beide die posisie van die rpoB mutasie, asook die genetiese agtergrond van die organisme, ’n belangrike rol speel in die uitdrukking van gene in rifampisin weerstandige M. tuberculosis. Kulture wat aan die kritiese konsentrasie van rifampisien vir 24 uur blootgestel is, het teenverwagting geen differensiële geen-uitdrukking getoon nie. Verder het die heel genoom volgorde bepaling van die in vitro mutante getoon dat sinonieme en nie-sinonieme enkel-nukleotied polimorfismes teenwoordig is in die onderskeie rpoB mutante. Dit dui daarop dat die mikobakteriële genoom voortdurend verander, moontlik nie so stadig as wat voorheen vermoed is nie.
Die bevindinge van hierdie navorsing bied nuwe insigte om die invloed van mutasies wat middel-weerstandigheid veroorsaak op die biologie van M. tuberculosis te verstaan. Dit het ook getoon dat verdere studies dringend nodig is om die komplekse fisiologie van hierdie patogeen te verstaan. Hierdie kennis sal van kardinale belang wees vir die sukses van toekomstige ondernemings om nuwe anti-tuberkulose middels te ontwikkel.
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Branham-O'Connor, Melissa. "Gene expression profile of tumor cell-fused or Noni (Morinda citrifolia)-treated dendritic cells." Connect to this title online, 2009. http://etd.lib.clemson.edu/documents/1263398967/.
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Cunha, Bianca Rodrigues da. "Investigação do perfil de expressão gênica e protéica de componentes do microambiente tumoral." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/41/41131/tde-02042012-110841/.
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Tem se tornado evidente que a iniciação e a progressão do câncer depende de vários componentes do microambiente tumoral, incluindo células inflamatórias e imunes (linfócitos, macrófagos e mastócitos), fibroblastos, células endoteliais, adipócitos e matriz extracelular. De maneira geral, esses componentes são conhecidos como estroma. Tanto interações pró- como anti-tumor ocorrem entre um câncer e suas células vizinhas. Em um estudo prévio, avaliamos dados de bibliotecas SAGE de carcinoma epidermóide de cabeça e pescoço (CECP) usando ferramentas estatísticas e de bioinformática e pudemos identificar os genes mais e menos expressos em tumores metastáticos versus não metastáticos e em tumores versus tecidos normais. Em outro estudo, avaliamos fatores parácrinos solúveis produzidos por células do estroma e por células neoplásicas que poderiam influenciar proliferação e expressão gênica e protéica. Ambos os estudos identificaram marcadores potenciais associados a respostas inflamatórias ou imunes. Dezenove desses genes foram selecionados por PCR em tempo real e o estudo foi realizado nas linhagens SCC-9 de células epiteliais neoplásicas e de fibroblastos isolados de um câncer oral, e em 40 amostras de carcinomas primários de cabeça e pescoço (6 amostras micro e 34 macrodissecadas). Nós também utilizamos eletroforese unidimensional para analisar a expressão protéica nesse conjunto de amostras. Como a microdissecção produziu baixas concentrações de RNA e proteínas, ciclos extras de amplificação de mRNA foram necessários para obter material suficiente para experimentos de PCR. Nossos dados mostraram que os perfis de expressão foram provavelmente pouco preservados durante os ciclos extras de amplificação. Em amostras macrodissecadas, nós consistentemente observamos que o nível de transcritos de MGLL, COX2, EP3, EP4 e LTAH4 estava reduzido, porém presente nas suas margens cirúrgicas. Os dados não confirmaram, em células de CECP, a hipótese de que MGLL produz menssageiros lipídicos oncogênicos, esta via pode não atuar nesses pacientes. Nós também observamos que metaloproteinases são expressas em níveis elevados em CECP e devem estar envolvidas na degradação da matriz extracelular. Células neoplásicas e do estroma desses carcinomas exibem uma ampla variedade de proteínas com níveis muito diferentes de expressão. Este resultado abre perspectivas para realização de experimentos de validação<br>It has become evident that cancer initiation and progression depends on several components of the tumor microenvironment, including inflammatory and immune cells (lymphocytes, macrophages and mastocytes), fibroblasts, endothelial cells, adipocytes, and extracellular matrix. Collectively, these components are known as the stroma. Both pro- and anti-tumor interactions occur between a tumor and its surrounding cells. In a previous study, we evaluated data from SAGE libraries of head and neck squamous cell carcinoma (HNSCC) using statistical and bioinformatic tools and we could identify top-up and top-downregulated genes in metastatic versus non-metastatic tumors and in tumors versus normal tissues. In another study, we evaluated soluble paracrine factors produced by stromal and neoplastic cells which may influence proliferation and gene and protein expression. Both studies identified potential markers associated with immune or inflammatory response in head and neck tumorigenesis. Nineteen of these genes were selected for real-time polymerase chain reaction (PCR) and the study was carried out on the epithelial cancer cell line SCC-9 and on fibroblasts isolated from an oral cancer, and in 40 samples from primary HNSCC (6 micro and 34 macrodissected samples). We also used one-dimensional gel electrophoresis and mass spectrometry to analyze protein expression in this set of samples. As microdissection yielded low RNA and protein concentrations, extra rounds of mRNA amplification were necessary to obtain sufficient material for PCR experiments. Our data showed that expression profiles were probably scantily preserved during the extra rounds of amplification. In macrodissected samples, we consistently observed that the level of MGLL, COX2, EP3, EP4 e LTAH4 transcripts was low in most tumors but present in their surgical margins. The data do not confirm in HNSCC the hypothesis that MGLL produces oncogenic lipid messengers, this pathway may not act in these patients. We also observed that metalloproteinases are overexpressed in HNSCC and should be involved in extracellular matix degradation. Neoplastic and stromal cells from HNSCC exhibit a wide variety of proteins with very different levels of expression. This result opens the perspective to perform validation experiments.
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Brooks, Geoffrey Lance. "Coelomic Fluid Protein Profile in Earthworms Following Bacterial Challenge." Thesis, University of North Texas, 2006. https://digital.library.unt.edu/ark:/67531/metadc5476/.
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Proteomic techniques were used to evaluate the protein profile of the earthworm, (Lumbricus terrestris), following a bacterial challenge. One control group received no injection; a second control group received injections of phosphate buffer solution (PBS). The experimental group received injections of PBS containing (Aeromonas hydrophila). After incubation for 12 hours at 20°C, coelomic fluid was collected from each group for analysis by 2-D electrophoresis. There were significant differences in spot appearance and density between control and experimental groups. Sixteen spots showed a two-fold increase in density and 63 showed at least a two-fold decrease in density between samples from control and bacteria-challenged earthworms, respectively, suggesting up- and down-modulation of proteins potentially involved in the earthworm's response to bacterial challenge.
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Li, Zheng. "Profile of expression of ADAMTS, TIMP genes and translational control of ADAMTS in RPE cells." Thesis, University of Newcastle Upon Tyne, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.438498.
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Capper, David. "In vivo expression profile of XIAP and Smac protein in gliomas and correlation with prognosis." [S.l. : s.n.], 2008.
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Nicol, Moira Ruth. "Steroid secretory profile and steroidogenic acute regulatory (StAR) mRNA expression in cultured bovine adrenocortical cells." Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/23137.
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ACTH is the principal factor stimulating the formation and release of cortisol from the adrenal cortex and is controlled, in part, by the negative feedback inhibition of cortisol. Investigation into the kinetics of cortisol production by cultured bovine adrenocortical cells in response to ACTH-treatment and the relationship between the cortisol secretion and the expression of the steroidogenic acute regulatory (StAR) mRNA was undertaken. ACTH (10nM) treatment of BAC cells on day 3 of culture displayed an increase in the rate of cortisol output over the initial 6 hours, P<0.05 at each time point compared with untreated cells, followed by a marked decline in the secretion rate thereafter. The decline in the cortisol secretion rate was not due to a decrease in the number of cells as the protein content of the culture wells did not vary by ore than 10% over the 12 hour period. Nor was the decrease in cortisol secretion a result of serum-deprived culture as a comparable response was seen in serum-replete conditions. HPLC analysis of the culture medium revealed the secretion of four main steroids; cortisol, corticosterone, cortisone and 11β-hydroxyandrostenedione. Cortisol was found to account for ~ 50% of the total steroid output by BAC cells at each of the time points studied. The total steroid output increased over the initial 6 hours (6.1nmol/10<sup>6</sup> cells at 6 hours) followed by a decline in levels to 4.4nmol/10<sup>6</sup> cells at 12 hours. Thus, the decline in cortisol secretion was not due to the production of another steroid in preference to cortisol. Various concentrations of ACTH also invoked a similar pattern of cortisol secretion as did treatment of BAC cells with angiotensin II. Interestingly, no decline in cortisol secretion was found when BAC cells were treated with forskolin or 8Br-cAMP. Receptor desensitisation was ruled out as the cells responded to a second ACTH-treatment.
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Zhou, Tong, Haiyang Tang, Ying Han, et al. "Expression profile of mitochondrial voltage-dependent anion channel-1 (VDAC1) influenced genes is associated with pulmonary hypertension." KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY, 2017. http://hdl.handle.net/10150/624396.
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Several human diseases have been associated with mitochondria! voltage-dependent anion channel-1 (VDAC1) due to its role in calcium ion transportation and apoptosis. Recent studies suggest that VDAC1 may interact with endothelium-dependent nitric oxide synthase (eNOS). Decreased VDAC1 expression may limit the physical interaction between VDAC1 and eNOS and thus impair nitric oxide production, leading to cardiovascular diseases, including pulmonary arterial hypertension (PAH). In this report, we conducted meta-analysis of genome-wide expression data to identify VDAC1 influenced genes implicated in PAH pathobiology. First, we identified the genes differentially expressed between wild-type and Vdac1 knockout mouse embryonic fibroblasts in hypoxic conditions. These genes were deemed to be influenced by VDAC1 deficiency. Gene ontology analysis indicates that the VDAC1 influenced genes are significantly associated with PAH pathobiology. Second, a molecular signature derived from the VDAC1 influenced genes was developed. We suggest that, VDAC1 has a protective role in PAH and the gene expression signature of VDAC1 influenced genes can be used to i) predict severity of pulmonary hypertension secondary to pulmonary diseases, ii) differentiate idiopathic pulmonary artery hypertension (IPAH) patients from controls, and iii) differentiate IPAH from connective tissue disease associated PAH.
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Ding, Peihui, and 丁佩惠. "Expression profile, molecular regulation and immuno-inflammatory function of LPS-binding protein in human oral keratinocytes." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B49617795.
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Lipopolysaccharide (LPS)-binding protein (LBP) functions as a crucial molecule in innate immune responses to bacterial challenge. Our recent study shows the expression of LBP in human gingiva and its significant association with periodontal condition. Porphyromonas gingivalis is a keystone periodontopathogen with its LPS as a major virulence factor strongly involved in periodontal pathogenesis. Recent study has discovered that P. gingivalis LPS displays a significant lipid A structural heterogeneity. The present study investigated i) the expression profile of LBP in human oral keratinocytes (HOKs) stimulated by P. gingivalis LPS with penta-acylated (LPS1690) and tetra- (LPS1435/1449) lipid A structures as well as E. coli LPS; ii) the involvement of toll-like receptors (TLRs) and downstream signaling mechanisms in LBP expression; and iii) the effects of LBP and its crosstalk with the two isoforms of P. gingivalis LPS on the expression of cytokines and human β-defensins (hBD-2) in HOKs.
The expression of LBP mRNA and peptide was significantly up-regulated by P. gingivalis LPS1690 and E. coli LPS, while not by P. gingivalis LPS1435/1449. P. gingivalis LPS1690-induced LBP expression was through both TLR2 and TLR4, and the relevant down-stream signaling mechanisms were then further investigated. Western blot results showed that P. gingivalis LPS1690 activated the phosphorylation of IκBα, p65, p38 MAPK and SAPK/JNK, whereas E. coli LPS phosphorylated IκBα, p38 MAPK and SAPK/JNK. A nuclear translocation of NF-κB transcription factor was confirmed upon stimulation by both forms of LPS. Further blocking assay revealed that P. gingivalis LPS1690 induction of LBP was through NF-κB and p38 MPAK pathways, while E. coli LPS induction of LBP was mediated by NF-κB, p38 MPAK and JNK pathways. The effects of LBP and its crosstalk with P. gingivalis LPS1690 or LPS1435/1449 on the expression of cytokines and hBD-2 were further investigated. Interestingly, recombinant human LBP (rhLBP) per se could significantly up-regulate the expression of IL-6, IL-8 and TNF-α, while down-regulate hBD-2 expression. P. gingivalis LPS1690 or LPS1435/1449 modulated to different extents the rhLBP-induced cytokine expression. Notably, P. gingivalis LPS1690 significantly down-regulated rhLBP-induced IL-8 expression; whereas, P. gingivalis LPS1435/1449 down-regulated IL-8 expression more intensively (around 80% vs. 40% reduction). The key mediators of TLRs and their adaptors like CD180 and MD-1 were significantly down-regulated by rhLBP (fold changes: -2.44 and -9.62, respectively). Both CD180 and MD-1 mRNAs were up-regulated by P. gingivalis LPS1435/1449 (7.11 and 4.05 folds, respectively); while these two genes were reversely modulated by P. gingivalis LPS1690 (20.86 and -6.93 folds, respectively).
The present study demonstrates that P. gingivalis LPS with a lipid A structural heterogeneity differentially modulates LBP expression in HOKs. P. gingivalis LPS1690 promotes LBP expression in HOKs through TLR2 and TLR4 as well as NF-κB and p38 MAPK pathways in a way different from E. coli LPS. rhLBP per se significantly up-regulates the expression of IL-6, IL-8 and TNF-α, while down-regulates hBD-2 expression. P. gingivalis LPS with different lipid A structures down-regulates to different extents the rhLBP-induced expression of cytokines in HOKs, likely through fine-tuning of the CD180-MD1 complex and the relevant TLRs.<br>published_or_final_version<br>Dentistry<br>Doctoral<br>Doctor of Philosophy
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D’Anello, Laura <1980>. "Epigenetic control of the basal-like gene expression profile via Interleukin-6 in breast cancer cells." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2011. http://amsdottorato.unibo.it/3368/.
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Chen, Chang-Chin, and 陳長親. "Characterization of gene expression profile in erythropoiesis." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/74xyv5.
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碩士<br>慈濟大學<br>分子生物暨人類遺傳學系碩士班<br>102<br>A complex and incurable leukemia disease, myelodysplastic syndrome (MDS), is always a course in clinical. The patients who suffered from MDS may be developing refractory anemia finally. Nowadays, flow cytometry is developed for diagnosis and prognosis of lymphoproliferative and myeloproliferative disorders; however, the difficulty of standardizing flow cytometry diagnosis has increased because of insufficient specific clusters of differentiation (CD) markers of every erythroid stage for dyserythropoiesis disorders. In this study, 3 known CD markers (CD45, CD71, and CD235a) were used to gate 4 normal bone marrow erythroid differentiation groups. The first group is mainly the erythroblast and the basophilic normoblast (CD45dim/low/CD71dim/bright/CD235a–) (about 2 to 5% of all erythroid populations). The second group comprises mostly the polychromatophilic normoblast and the orthochromatophilic normoblast (CD45-/CD71bright/CD235a+), which occupies the highest cell proportion of all erythroid populations (80 to 90%). The third group is mainly the reticulocyte (CD45-/CD71dim/CD235a+), which occupies the lowest cell proportion (less than 1%). The fourth group is mainly the mature erythrocytes (CD45-/CD71-/CD235a+) (about 0 to 20%). After analyzing the samples from MDS patients, our results showed that the expression of CD71 was reduced in the second group. In order to find out more novel erythroid differentiation markers to delineate the erythropoiesis defect in 4 MDS patients, the first and second group erythroid cells of humans and mice were sorted for microarray and gene ontology analysis. Then, erythroid cell membrane related candidate genes were selected, and the MetaCore software was also used to identify novel CD71-related CD markers. The results showed CD36 and many other cell surface markers will be used to help the clinical diagnosis for MDS patients. Furthermore, these markers also will be helpful for distinguishing erythropoiesis stages.
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Huang, Chih-hua, and 黃之華. "CDK2AP1 Expression Profile in Oral Cancer Prognosis." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/xfjj2j.
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碩士<br>國立中山大學<br>生物醫學科學研究所<br>95<br>Oral cancer is now the fourth leading cause of male cancer mortality in Taiwan. Betel quid chewing is one of the main causes of oral cancer in Taiwan. CDK2AP1 is a growth suppressor gene that negatively regulates cyclin-dependent kinase 2 (CDK2) activities. Expression of p12CDK2AP1 protein is reduced and/or lost in oral cancers. Mutations in microsatellite-like sequence of CDK2AP1 gene in microsatellite instability colorectal cancer are associated with down-regulated CDK2AP1 transcription. This mutation was due to down-regulation of one DNA repair protein, MLH1. In order to understand whether CDK2AP1 mRNA and protein expression levels associate with betel-chewing oral cancers, we firstly analyzed 44 oral cancer specimens (normal and tumor, in pairs) by quantitative reverse transcription polymerase chain reaction and Western blotting. Immunohistochemistry was used to examine p12CDK2AP1 protein expression in another 167 buccal mucosa squamous cell carcinoma tissues. We have demonstrated that the expression levels of CDK2AP1 mRNAs were slightly higher in normal oral tissues than those in tumor tissues (P>0.05). Similarly, p12CDK2AP1 and CDK2 protein expression levels were up-regulated in oral cancer tissues than in normal tissues by Western blot analysis (P<0.05). Among Ca9-22, CAL27, SAS and in betel-chewing oral cancer cells TW2.6 and human normal skin keratinolial cells (HaCaT) that we examined, p12CDK2AP1 and CDK2 proteins were detected to be highest expressed in Ca9-22 and TW2.6 cells, respectively, when compared to HaCaT cells. Immunocytochemistry indicated p12CDK2AP1 expressed in nucleus and cytoplasm in Ca9-22, CAL27, SAS and HaCaT cells, however predominant present in nucleus in TW2.6 cells. On the other hand, immunohistochemistry demonstrated that nuclear (P=0.157) and cytoplasmic p12CDK2AP1 (P=0.350) in 167 patients with buccal mucosa squamous cell carcinoma were slightly down-regulated. Reduction of nuclear p12CDK2AP1 was not significantly correlated with any clinicopathologic characteristics or prognosis. Direct sequencing indicated that lack of microsatellite-like instability of CDK2AP1 3’-UTR in four oral cancer cell lines, HaCaT and six patients with down-regulated MLH1 protein. In conclusion, we demonstrated that: (1) p12CDK2AP1 was located in both the nucleus and cytoplasm in most oral cancer cell lines and HaCaT cells but predominate present in the nucleus in betel-chewing oral cancer cells, TW2.6; (2) Reduction of nuclear p12CDK2AP1 in buccal mucosa squamous cell carcinoma tissues were identified, however, not significantly correlated with any clinicopathologic characteristics, prognosis or betel chewing; (3) In six patients with down-regulated MLH1, lack of micorsatellite-like instability in the CDK2AP1 3’-UTR region has been found.
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Wu, Miin-feng, and 吳敏鳳. "Expression Profile Analysis of Hsc70 of Vigna raiata." Thesis, 2001. http://ndltd.ncl.edu.tw/handle/91186420244138748697.
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碩士<br>國立清華大學<br>生命科學系<br>89<br>When facing upon various kinds of stresses such as heat, cold, wounding, heavy metals, and water deficit, organisms usually synthesize molecular chaperons to cope with stress. The seventy kilodalton heat shock protein (HSP70) and the constitutively expressing heat shock cognate (HSC70) are conserved among all organisms. In addition to stress-induction, HSP/HSC70 have been found to be up-regulated at specific development stages in the absence of stress. Previous studies in our laboratory showed that a HSP/HSC of about 71 kDa is expressed in germinating mung bean (Vigna radiata) seedlings. In order to investigate the expression profile of Hsc70 in mung bean, a cDNA library was constructed from mRNAs isolated from mung bean seedlings at 3 days after germination (dag). Three heat shock protein genes were isolated from the library and designated as VrHsc70-1, VrHsc70-2, and VrHsc70-3. The expression profiles of these genes were analyzed with Northern blots analyses and RNase protection assays using the [-32P] UTP labeled antisense RNA as gene-specific probes. The levels of VrHsc70-1, VrHsc70-2 and VrHsc70-3 mRNAs increased from 0 dag to 3 dag and maintained until 7 dag. During embryogenesis, the mRNA levels of these three genes was substantial from 0 to 15 days after anthesis (daa) and declined remarkably at 25 daa. The expression of VrHsc70-1 mRNA was significantly induced by cold (4oC) and heat (37oC) treatments, while VrHsc70-2 and VrHsc70-3 mRNAs were only slightly induced by heat. Our results indicate that the expression of these three genes might not be related to seed maturation and desiccation during late embryogenesis. Although these three genes are constitutively expressed, the expression of VrHsc70-1 is apparently regulated by temperature stress.
Abstract ‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧ii
謝誌‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧iv
List of Figures ‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧v
Abbreviations ‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧vi
Table of Contents‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧vii
Introduction ‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧1
Materials and Methods ‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧8
1. Plant growth ‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧8
2. Stress treatments ‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧8
3. Total cellular RNAextraction ‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧9
4. cDNA library construction ‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧11
5. cDNA library screening ‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧20
6. Mini-scale plasmid DNA preparation ‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧23
7. DNA sequencing‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧24
8. Large-scale plasmid DNA preparation‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧25
9. Amplifying the 5’ end of cDNA by reverse transcription and polymerase chain reaction (PCR) ‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧27
10.Amplifying the 3’ untranslated sequences by polymerase chain reaction‧‧‧‧28
11. Synthesis of single stranded RNA probes by in vitro transcription‧‧‧‧‧‧29
12. Northern blot analysis‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧ 30
13. RNase protection assay‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧31
Results ‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧33
Discussion ‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧39
Figures ‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧42
References ‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧‧53
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Lee, Tzong-Yu, and 李宗祐. "Expression Profile of MicroRNAs in Glioblastoma Multiforme Tissues." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/77242398008874775696.
Full textAbstract:
碩士<br>中國醫藥大學<br>免疫學研究所碩士班<br>99<br>Glioblastoma multiforme (GBM), is highly aggressive with a median survival of one year, even with the most effective combined therapies. MicroRNAs (miRNAs) are short endogenous noncoding RNAs that silence the production of proteins by binding to mRNA 3’UTR regions. miRNAs have been shown their roles in the regulation of biological properties in glioblastomas, including cell proliferation, invasion, cancer stem cell growth, and angiogenesis. In this study, we compared the expression levels of microRNAs between clinic GBM tissues and normal brain tissues. For acquiring the profiles of different expression levels of global miRNAs, 7 clinic samples from GBM patients, 1 normal brain tissue and 2 primary cells derived from GBM tissues were processed and analyzed by use of the miRNAs microarray system. In our results, expression levels of 13 microRNAs were shown to downregulate significantly in GBM tissue samples. These results from miRNA array analysis were also confirmed by use of qRT-PCR analysis. The expression levels of 6 miRNAs were the same as the findings in the miRNA array system. In summary, a panel of differentially expressed miRNAs derived from the microRNAs expression profile may serve as the potential molecular biomarkers for the therapy target of glioblastoma. By use of computational algorithm, we further predicted potent genes which are targeted by 13 miRNAs. And use published DNA microarray database in GBM to distinguish the genes affected by miRNAs. Some of predicted genes had been shown to play key functions in proliferation, cell cycle, development, cell survival and migration. And further studies to investigate the effect of these miRNAs on glioblastomas biology are necessary.
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Pantazi, Angeliki. "microRNA expression profile of undifferentiated and differentiating pluripotent cells." Doctoral thesis, 2009. http://hdl.handle.net/11858/00-1735-0000-0006-AF62-2.
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Chen, Emily, and 陳曉怡. "Pattern Recognition of Gene Expression Profile in Function Group." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/58004287004496613670.
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Tsai, Hong-Yuan, and 蔡弘原. "Expression profile of TSG101 protein and it，s phosphorylationstatus." Thesis, 2003. http://ndltd.ncl.edu.tw/handle/93520731654307712529.
Full textAbstract:
碩士<br>國立中山大學<br>生物科學系研究所<br>91<br>Functional inactivation of tumor susceptibility gene tsg101 leads to cellular transformation and tumorigenesis in mice. No genomic DNA deletion in TSG101gene in human cancer indicated TSG101 is not a typical tumor suppressive gene. TSG101 participates in the MDM2/p53 feedback control loop and the regulation of the cellular membrane trafficking. However, detail functional characteristics remains to be elucidate.
In this study, we explored the tsg101 expression in adult mouse tissues from various organs using immunohistochemistry and in situ hybrid- ization. The results indicated that tsg101 expression was ubiquitous but in differential steady-state level in various cell types. The expression of tsg101 mainly found in epithelial cells、secretory cells and nerve cells. The second topic of this study was to characterize the phosphorylation status of TSG101 protein. Endogeneously expressed TSG101 and exogeneously expressed HA-tag TSG101 protein were purified by immunoprecipiation with #820 antiserum against TSG101, and were subjected for western blot analysis using anti-phosphoserine and anti-phosphothreonine antibodies. This experiment had confirmed that TSG101 protein contained both phosphoserine and phosphthreonine residues. In vitro kianse assay using GST-tag and his-tag TSG101 funsion proteins was exploited to investigate the kinase responsible for TSG101 phosphorylation. The results clearly indicated that cdc2、GSK3β and PKC kinases could phosphorylate TSG101 fusion Protein, implying that the function of TSG101 might be regulated by the signaling involving these kinases.
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Huang, Yi-Huei, and 黃怡慧. "Gene expression profile of U937-cell stimulated by mannan conjugate." Thesis, 2003. http://ndltd.ncl.edu.tw/handle/98591064948644271903.
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碩士<br>臺北醫學大學<br>生物醫學技術研究所<br>91<br>During infection, mannose receptor of human macrophages play a important role in pathogenic detection and responses. Macrophages have a lot of effector functions induced via mannose receptor, including mediated phagocytosis of pathogens, induced cytokines secretion to regulate immune system, and increased reactive oxygen intermediates production to enhance cytotoxicity. In past several years, there are many researches about gene and protein structure of mannose receptor, but its molecular effects, even the initiated signal(s) of phagocytosis events, are not identified yet. Currently, advancement in methodology, researchers allows using high-throughput methods to investigate behaviors of the cell by systematic biology. In the present study, mannan conjugates was applied as mannose receptor ligands to allow us to examine effected genes by oligonucleotide microarray. A total of 5091 genes were altered in the mannan conjugate treatment as compared with control. The results were verified using real-time quantitative reverse-transcription polymerase chain reaction (RT-PCR). 80% consistence was acquired. Cellular protein expression level was further analyzed by two-dimensional electrophoresis and identified by ESI-Q-Tof. Based on the interaction between mannose receptor and mannosylated glycocojugates, as an approach details about the effect of mannose receptor on expression of genes and proteins, as well as the biological mechanism, are hopefully more well understood.
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Yeh, Jhun-Ming, and 葉郡銘. "Gene expression profile of hepatitis B virus-positive hepatocellular carcinomas." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/51988712564546157195.
Full textAbstract:
碩士<br>中國醫藥大學<br>環境醫學研究所<br>93<br>The aim of this study was to develop and validate a molecular index for the diagnosis of hepatocellular carcinoma (HCC) based on genes whose specificity and level of expression are the most discriminating for HCC. The level of expression of 30 genes was assessed by a real-time reverse transcription-polymerase chain reaction approach at Hep-G2, Huh7 and 4 HBV-positive HCCs. The most informative genes were selected as diagnostic indices. As a result, 9 out of the 30 genes were differentially expressed in HCC. Moreover, 5 out of these 9 genes were eventually selected according to their performance and univariate analysis results. A multivariate analysis was then used to obtain an expression for the diagnostic index by conditional logistic regression. Using a cut-off score of 65, sensitivity and specificity are 95% and 80%, respectively, in 20 HBV-positive HCCs. It may offer a basis for future studies on the differentiation of ambiguous cases with early-stage HCCs.
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Cheung, Jr K.-John J. "Expression profile and molecular functions of the tumor suppressor p33ING1." Thesis, 2003. http://hdl.handle.net/2429/14892.
Full textAbstract:
The biological functions of the tumor suppressor gene, ING1, have been studied extensively in the last few years since it was cloned. Four alternatively spliced forms of ING1, named p47[sup ING1], p33[sup ING1], p27[sup ING1], and p24[sup ING1], have been identified and found to share many biological functions with those of p53. Some of these isoforms have previously been reported to mediate growth arrest, senescence, apoptosis, anchorage-dependent growth, and chemosensitivity. Functions, such as cell cycle arrest and apoptosis, have been shown to be dependent on the activity of both ING1 and p53 proteins. In this thesis, we sought to characterize further a number of important biological functions of the p33[sup ING1] isoform. We first investigated how the expression of ING1 is regulated in normal and stress conditions. Using a p53-knockout mouse model and various cell lines differing in p53 status and cell type, we found that the expression of p33[sup ING1] is independent of p53 status and induced by ultraviolet (UV) irradiation in a dose-/time-dependent and tissue-specific manner. These findings subsequently prompted us to investigate if p33[sup ING1] plays a role in UV-stress response, such as repair of UV-damaged DNA. Using both in vitro (host-cell-reactivation assay) and in vivo (radioimmunoassay) methods, we found that p33[sup ING1] enhances the repair of UV-damaged DNA in collaboration with p53 in melanoma cells and that GADD45 may participate in the process. Next we investigated the molecular pathways of p33[sup ING1] enhancement in UV-induced apoptosis in melanoma cells using various survival and apoptotic assays. We demonstrated that overexpression of p33[sup ING1] increases the apoptotic rate in melanoma cells after UV irradiation and that p53 has a synergistic effect on this process. Moreover, we found that p33ING1 enhances the expression of endogenous Bax and alters mitochondrial membrane potential, suggesting that p33ING1 cooperates with p53 in UV-induced apoptosis via the mitochondrial cell death pathway in melanoma cells. Lastly, we examined the role of p33ING1 isoform in melanoma chemosensitivity because previous findings indicate that the isoform p24ING1 is capable of enhancing chemosensitivity in human fibroblasts. Using a number of survival and apoptotic assays to quantitate cell death in melanoma cells, we showed that neither overexpressing p33[sup ING1] alone nor coexpression of p33[sup ING1] and p53 had an effect on the frequency of cell death induced by the chemodrug, camptothecin. We therefore demonstrated that p33[sup ING1] does not enhance camptothecin-induced cell death in melanoma cells. In conclusion, we have elucidated in this thesis some of the novel functions of p33[sup ING1] and the importance of this gene in the context of tumor suppression.
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Cheng, Chia-Yeh, and 鄭佳曄. "Expression Profile of 53BP1 in Non-Small Cell Lung Cancer." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/53951549638427256339.
Full textAbstract:
碩士<br>國立中興大學<br>生物醫學研究所<br>94<br>The p53 binding protein 1 (53BP1) is a highly conserved DNA damage checkpoint protein in all eukaryotes. 53BP1 contains two BRCT domains, which are present in several proteins involved in DNA repair and DNA damage-signaling pathways. Upon DNA damage, 53BP1 rapidly relocalized to DNA double-strand breaks and forms discrete nuclear foci. It has been shown that 53BP1 is required for DNA damage checkpoint protein activation and tumor suppression. 53BP1 facilitates the end-joining repair and class-switch repair processes. Impaired function of DNA damage response gives rise to chromosomal instability that can result in tumorigenesis. Although the mechanism of 53BP1 has been proposed to prevent genomic instability and tumorigenesis, the detail is still unclear.
Our results showed that 53BP1 mRNA expression is nearly the same in 6 lung cancer cell lines. By western blot analysis, 53BP1 was expressed in 7 lung cancer cell lines. About 60-70% lung cancer tissue specimens expressed 53BP1 mRNA and protein. Interestingly, a high molecular weight protein－53BP1'' was highly expressed in H226 and MCF-7 cell lines. Furthermore, expression of 53BP1'' was markedly increased than 53BP1 after cisplatin treatment. Hence, our results suggest that the different forms of 53BP1 contain distinct biological significance and may play diverse role in tumorigenesis.