Thematische Bibliographien / Transgenic Mice / Dissertationen
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Dissertationen zum Thema „Transgenic Mice“

Autor: Grafiati
Veröffentlicht am 4. Juni 2021
Zuletzt aktualisiert am 9. Juni 2025

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1

Simard, Marie-Chantal. "Nef pathogenesis in transgenic mice." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103182.

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In order to study the functions of SIV Nef in vivo, in a small animal model, transgenic (Tg) mice expressing the SIVmac239 nef gene, under the control of the human CD4 gene promoter (CD4C) were generated. The transgene was found to be expressed in the same cells targeted by the virus, in vivo. These CD4C/SHIV-nef SIV Tg mice develop a severe AIDS-like disease, including premature death, failure to thrive/weight loss, wasting, thymic atrophy, exhibit an especially low number of peripheral CD8+ T cells as well as low number of peripheral CD4+ T cells, diarrhea, splenomegaly, kidney (interstitial nephritis, segmental glomerulosclerosis), lung (lymphocytic interstitial pneumonitis) and heart disease. In addition, these Tg mice fail to mount a class-switched antibody response after immunization with ovalbumin, produce anti-DNA autoantibodies and some of them develop P. Carinii lung infection. These CD4C/SHIV-nefSIV Tg mice develop an AIDS-like disease very similar to that of CD4C/HIV Tg mice, except that the kidney and cardiac diseases were more severe, and that a thymic developmental defect was observed. Heart enlargement was very severe in CD4C/SIV Tg mice during early breeding on the C3H background. Histopathological lesions in the heart of these mice were also multifocal and were similar to those found in CD4C/HIV Tg mice. Data from echocardiography analysis are not yet available for these Tg mice. The low number of peripheral CD8+ and CD4 + T cells likely reflects a thymic defect and may be similar to the DiGeorge-like "thymic defect" immunophenotype described in a subgroup of HIV-1 infected children. Ontogeny studies show that the Tg mice were born with a smaller thymus and that this phenotype is not progressive in nature. As young as embryonic day 17, the thymic absolute cell numbers are lower in the Tg mice when compared to their non-Tg controls and there is a defect in thymocyte maturation in the transition between DN3 and DN4, with a failure to generate normal numbers of DP cells. Fetal liver transplantation studies have ruled out a significant impairment of the thymic epithelium and have suggested that this defect is likely a direct consequence of abnormal T cell progenitors in the thymus.<br>Therefore, it appears that SIV Nef alone expressed in mice, in appropriate cell types and at sufficient levels, can elicit many of the phenotypes of simian and human AIDS. These Tg mice should be instrumental in studying the pathogenesis of SIV Nef-induced phenotypes.
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2

Husbands, Sandra D. "Tolerance and immunity in transgenic mice." Thesis, University College London (University of London), 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303680.

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3

Cosentino, Lidia. "A comparison of transgenic and endogenous loci in vivo." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0018/NQ56223.pdf.

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4

Malmström, Vivianne. "Arthritis susceptibility and tolerance in collagen transgenic mice." Lund : Dept. of Cell and Molecular Biology, Section for Medical Inflammation Research, Lund University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/38986502.html.

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5

So, Chi-leung. "Transgenic mouse model of human chondrodysplasia /." Hong Kong : University of Hong Kong, 1997. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19161347.

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6

Gratao, Ana Angélica. "Impaired fertility in transgenic mice overexpressing betacellulin." [S.l.] : [s.n.], 2007. http://edoc.ub.uni-muenchen.de/archive/00006575.

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7

Gratao, Ana Angelica. "Impaired Fertility in Transgenic Mice Overexpressing Betacellulin." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-65751.

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8

Felmer, R. "Genetic manipulation of fat in transgenic mice." Thesis, University of Edinburgh, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.650832.

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The present dissertation describes the use of a novel system to achieve specific cell ablation in fat tissue. The method is based on the use of <i>E.coli</i> nitroreductase (NTR) enzyme that activates certain nitro compounds into cytotoxic DNA interstrand cross-linking agents. This system was assessed first <i>in vitro,</i> in a preadipocyte cell line (3T3L1). Clones of cells that expressed NTR were successfully killed after treatment with CB1954. It was confirmed that the mechanism of cell killing involved is apoptosis and the presence of a cell-permeable metabolite that is released to the medium triggering a bystander effect was observed. This prodrug system was also assessed <i>in vivo</i>, for which transgenic mice were generated expressing NTR specifically in adipose tissue under the control of the aP2 promoter. Upon CB1954 treatment, transgenic mice showed extensive cell depletion in different fat deposits, which was directly correlated to both the dose of prodrug and the levels of NTR expressed. The present model provides a new inducible approach to manipulate the number of adipocytes at different stages of the mouse development and provides a new system for the study of fat metabolism especially in abnormal conditions such as obesity and its modulation through the manipulation of the target cell population. Also reported are preliminary experiments to assess a novel system of ablation mediated by the murine adapter molecule RAIDD. Stable cell lines were generated to overexpress RAIDD after differentiation. A range of phenotypes was observed with these clones from a complete blockage of the differentiation to the killing of cells that escape the blockage. The present results suggest for first time a new developmental role for this gene and strongly encourage further experimentation to confirm this effect in an experimental animal model.
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9

Cox, April. "Effects of hyperoxia in alzheimers transgenic mice." Scholar Commons, 2005. http://scholarcommons.usf.edu/etd/2836.

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An association between major surgery in the elderly and precipitation of Alzheimers disease (AD) has been reported. Hyperoxia (100%) oxygen is commonly administered after surgery to increase the oxygen content of blood. However, hyperoxia is a potent cerebral vasoconstrictor and generator of free radicals, as is [beta]amyloid (A[beta];). This study was aimed at examining behavioral, neuropathological, and neurochemical effects of hyperoxia treatments in APPsw transgenic mice (Tg+), which have elevated brain A[beta]; levels by 3-4 months of age but are not yet cognitively-impaired. At 3 months of age, Tg+ mice were pre-tested in the radial arm water maze (RAWM) task of working memory and found to be unimpaired. At 4.5 months of age, half of the Tg+ mice received the first of 3 equally-spaced hyperoxia sessions (3 hrs each) given over the ensuing 3 months. The other half of the Tg+ mice were exposed to compressed air during these 3 sessions. RAWM testing performed immediately following the final gas session at 7.5 months of age revealed significant working memory impairment in Tg+ mice exposed to hyperoxia. The Tg+ group that was exposed to placebo treatment showed a trend towards impairment, however, was not significantly different from the non-transgenic group. Hyperoxia-induced memory impairment in Tg+ mice did not involve changes in brain A[beta] deposition, degenerative cell numbers in hippocampus, neocortical lipid peroxidation, or hippocampal levels of APP, ApoE, COX-2, or GFAP. The combination of excess A[beta] and hyperoxia could have induced greater oxidative stress and cerebral vasoconstriction than either one alone, resulting in a pathologic cerebral hypoperfusion that triggered subsequent cognitive impairment.
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10

Calver, Andrew Robert. "Oligodendrocyte population dynamics : insights from transgenic mice." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322239.

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11

Derrett-Smith, E. C. "Systemic sclerosis vasculopathy : exploration in transgenic mice." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1383812/.

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Vascular disease in systemic sclerosis (SSc) leads to significant morbidity and mortality. No robust animal model of vasculopathy in SSc has been described. The hypothesis underpinning work described in this thesis is that a primary defect in TGFβ signalling is sufficient to generate the fibrotic, vascular and inflammatory phenotype of this condition. This is explored using a novel transgenic mouse model of SSc (TβRIIΔk-fib). The transgenic mouse strain TβRIIΔk-fib carries a kinase-deficient type II TGFβ receptor which is expressed under the control of a fibroblast specific promoter leading to balanced ligand-dependent upregulation of TGFβ signalling. Consequent increased TGFβ ligand in the peri-fibroblast microenvironment modulates other cell types. The phenotype is one of ubiquitous skin and gut fibrosis and increased susceptibility to severe and persistent fibrosis in response to epithelial lung injury. In this thesis, a cardiovascular phenotype is characterised for the first time, with adventitial fibrosis and medial attenuation within the large elastic arteries of the systemic circulation resulting in systemic hypertension with cardiac fibrosis. Within the pulmonary arterial circulation, there is ubiquitous medial hypertrophy, perivascular inflammation and mild pulmonary hypertension. In both circulations, the phenotype can be exaggerated additional vascular stress: NO synthase inhibition results hypertensive renal stress and VEGFR2 inhibition results in obliterative vascular changes representative of pulmonary arterial hypertension. This thesis demonstrates a unique phenotype that is strikingly relevant to that of human SSc vasculopathy, providing compelling evidence for the role of altered TGFβ signaling in systemic and pulmonary vasculopathy and for the role of altered cell interactions and responses to injury in the development of vascular consequences. A paradigm in which a background TGFβ dependent vasculopathy renders mice susceptible to injury leading to hallmark features of SSc vasculopathy is suggested. This model provides mechanistic insight and a potential platform for preclinical interventional studies in these important complications of SSc.
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12

蘇志良 and Chi-leung So. "Transgenic mouse model of human chondrodysplasia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31237678.

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13

衛永剛 and Wing-kong Wai. "Abnormal chondrocyte differentiation: a transgenic model." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31237800.

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14

Wai, Wing-kong. "Abnormal chondrocyte differentiation : a transgenic model /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19656439.

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15

Thomas, Alysia D. "Endocrine mechanisms for reproductive failure and transgene transmission in oMt1a-oGH transgenic mice /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2003. http://uclibs.org/PID/11984.

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16

Myelnikov, Dmitriy. "Transforming mice : technique and communication in the making of transgenic animals, 1974-1988." Thesis, University of Cambridge, 2015. https://www.repository.cam.ac.uk/handle/1810/252737.

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17

Lemon, Jennifer Rollo C. David. "Oxidative stress and aging processes in transgenic growth hormone mice." *McMaster only, 2005.

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18

Oghumu, Steve Onyeka. "Generation and Characterization of CXCR3 Bicistronic Reporter Mice and CXCR3 Transgenic Mice." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1274927351.

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19

Rizzo, Stefania. "Arrhythmogenic cardiomyopathy: electrical instability and intercalated disc abnormalities in transgenic mice." Doctoral thesis, Università degli studi di Padova, 2013. http://hdl.handle.net/11577/3426181.

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Aims: Mutations in genes encoding desmosomal proteins have been implicated in the pathogenesis of arrhythmogenic right ventricular cardiomyopathy (ARVC). However, the consequences of these mutations in early disease stages are unknown. We investigated whether mutation-induced intercalated disc remodeling impacts on electrophysiological properties before the onset of cell death and replacement fibrosis. Methods and Results: Transgenic mice with cardiac overexpression of mutant Desmoglein2 (Dsg2) Dsg2-N271S (Tg-NS/L) were studied before and after the onset of cell death and replacement fibrosis. Mice with cardiac overexpression of wild-type Dsg2 and wild-type mice served as controls. Assessment by electron microscopy established that intercellular space widening at the desmosomes/adherens junctions occurred in Tg-NS/L mice before the onset of necrosis and fibrosis. At this stage, epicardial mapping in Langendorff-perfused hearts demonstrated prolonged ventricular activation time, reduced longitudinal and transversal conduction velocities, and increased arrhythmia inducibility. A reduced action potential upstroke velocity due to a lower Na+ current density was also observed at this stage of the disease. Furthermore, co-immunoprecipitation demonstrated an in vivo interaction between Dsg2 and the Na+ channel protein NaV1.5. Conclusion: Intercellular space widening at the level of the intercalated disc (desmosomes/fascia adherens junctions) and a concomitant reduction in action potential upstroke velocity, as a consequence of lower Na+ current density, leads to slowed conduction and increased arrhythmia susceptibility at disease stages preceding the onset of necrosis and replacement fibrosis. The demonstration of an in vivo interaction between Dsg2 and NaV1.5 provides a molecular pathway for the observed electrical disturbances during the early ARVC stages.<br>Introduzione: Mutazioni nei geni che codificano per le proteine desmosomali giocano un ruolo fondamentale nella patogenesi della cardiomiopatia aritmogena del ventricolo destro (ARVC). Tuttavia, le conseguenze di tali mutazioni negli stadi precoci della malattia sono sconosciute. Scopo del nostro studio è stato di indagare se il rimodellamento dei dischi intercalari come conseguenza di mutazioni nelle proteine desmosomali modifichi le proprietà elettrofisiologiche cardiache prima dello sviluppo di morte cellulare e fibrosi sostitutiva. Metodi e Risultati: Topi transgenici con overespressione cardiaca della proteina Desmogleina2 mutata (Dsg2) -Dsg2-N271S (Tg-NS/L)- sono stati studiati prima e dopo lo sviluppo di morte miocitaria e fibrosi sostitutiva. Come controlli, abbiamo usato topi wild-type e topi con overespressione della Dsg2 normale. Studi di microscopia elettronica hanno evidenziato la presenza di spazi intercellulari allargati in corrispondenza delle giunzioni meccaniche desmosomi/giunzioni aderenti nei topi Tg-NS/L prima dello sviluppo di necrosi e fibrosi. Contemporaneamente, il mappaggio epicardico in cuori perfusi con soluzione Langendorff ha dimostrato prolungamento del tempo di attivazione ventricolare, riduzione della velocità di conduzione longitudinale e trasversale, ed aumento della inducibilità di aritmie. Inoltre, nello stesso stadio di malattia, si osservava ridotta velocità del potenziale d’azione dovuta a minore densità della corrente del sodio. Studi di co-immunoprecipitazione, infine, dimostravano un’interazione in vivo tra la Dsg2 e la proteina NaV1.5 dei canali del sodio. Conclusioni: Un allargamento degli spazi intercellulari a livello dei dischi intercalari e una concomitante riduzione del potenziale d’azione, come conseguenza di una minore corrente del sodio, portano ad un ritardo di conduzione ed ad aumentata suscettibilità aritmica negli stadi di malattia che precedono la necrosi e la fibrosi sostitutiva. La dimostrazione di un’interazione in vivo tra Dsg2 e NaV1.5 suggerisce una spiegazione a livello molecolare dei disturbi elettrici osservati negli stadi precoci dell’ARVC.
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20

Wootz, Hanna. "Amyotrophic Lateral Sclerosis – A Study in Transgenic Mice." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7342.

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21

Andäng, Michael. "Expression and function of ribozymes in transgenic mice /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4143-2/.

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22

Wang, Jianming. "Life without mitochondrial DNA : studies of transgenic mice /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4491-1/.

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23

Salem, Hatem. "Behavioural analysis of transgenic mice overexpressing gamma-synuclein." Thesis, Cardiff University, 2011. http://orca.cf.ac.uk/32398/.

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The alpha-synucleinopathies is a diverse group of diseases characterised by malfunctioning of alpha-synuclein protein. Parkinson’s disease is the most common of all alpha-synucleinopathies. Intracellular inclusions, like Lewy bodies and certain other abnormal structures are the pathological hallmarks of this group of neurodegenerative diseases. The main protein component of these structures is alpha-synuclien. Alpha-synuclein is a member of the synuclein family, which consists of 3 closely related proteins, alpha-, beta- and gamma-synucleins. Alpha-synuclein is more extensively studied because of its direct involvement in human diseases, while our knowledge about two other family members is very limited. Neither beta-synuclein, nor gamma-synuclein is a component of Lewy bodies and other pathological structures typical for neurodegenerative diseases.
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24

Scudamore, Owen. "Modelling Parkinson's disease with α-synuclein transgenic mice". Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/modelling-parkinsons-disease-with-alphasynuclein-transgenic-mice(2c799251-df3c-43f8-8b29-866d06179512).html.

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Parkinson's disease is a chronic, progressive, neurodegenerative movement disorder characterised by bradykinesia, tremor at rest, rigidity and postural instability. The pathological hallmark of the malady is a loss of dopaminergic nigrostriatal neurons, coupled with the inclusion of Lewy bodies and Lewy neurites within the axons and processes of remaining neurons. The exact cause of the disorder remains elusive; however, rare inherited forms of the disease have highlighted specific genes involved in pathogenic pathways that could be germane to sporadic cases. alpha-Synuclein is one such gene, wherein mutations and multiplications provoke abnormal folding and aggregation of the protein to induce pathology. The relevance of alpha-synuclein to sporadic Parkinson's disease is strongly supported by the fact that it is the primary component of Lewy bodies. This has prompted the development of numerous transgenic animals based on alpha-synuclein overexpression; however, none of the models to date represents a perfect replicate of the human Parkinsonian pathology. Indeed, the use of different promoters and transgenes in mice has led to various phenotypes coupled with non-specific, non-existent or late-onset neurodegeneration. Since the majority of alpha-synuclein found within aggregates in PD brain is phosphorylated, it has been postulated that this post-translational modification could be the aggravating factor that initiates aggregation; however, phosphorylation could also be a late event, which occurs after alpha-synuclein is sequestered into inclusions, but where it remains accessible by relevant kinases. In the literature, there is contrasting evidence suggesting that phosphorylated alpha-synuclein is either inductive or preventative of aggregation. Therefore I produced two inducible transgenic mice that would overexpress mutant human alpha-synuclein in Purkinje cells to investigate the in vivo affect of alpha-synuclein phosphorylation on aggregation. The two constructs both contained the PD-linked A53T mutation, in addition to either an S87A or an S129A mutation; the substitution of serine with alanine in these constructs blocks phosphorylation occurring at that position. The mice were then aged and characterised on both a behavioural and a histopathological level. Although at present (age: 16 months) neither of the two lines exhibits any obvious alpha-synuclein pathology, they both present with a seizure phenotype and exhibit significantly reduced horizontal and vertical movement than wild-type controls in the Actimot open field. A different theory for the pathogenesis of PD indicates a role for malfunctioning mitochondria and oxidative stress. In a third mutant line, I wanted to assess the impact of increased oxidative stress on alpha-synuclein aggregation in vivo. Therefore I crossed a previously characterised mouse model of PD with a line haplodeficient for SOD2. This gene codes for a mitochondrial enzyme that scavenges free radicals, thus normally protecting the mitochondria from oxidative stress. The pathology of the haplodeficient SOD2 alpha-synuclein mice was compared with that of wt SOD2 alpha-synuclein mice at an age of 16 months using a combination of Western-blot, PK-PET-blot and immunohistochemical techniques. A significant difference was detected between the two lines suggesting that SOD2 deficiency accelerated alpha-synuclein pathology.
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25

Emson, Claire Lucy. "Analysis of interleukin-13 function using transgenic mice." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624439.

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26

Downing, Alison. "Generation of Ren-2/SV40 TsTAg transgenic mice." Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/13711.

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27

Klomkleaw, Wuthichai. "ATF3 transgenic mice : structural analysis of cardiac myocytes /." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486457871785014.

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28

Yamada, Go. "Generation of Transgenic Mice Overexpressing a Ghrelin Analog." Kyoto University, 2011. http://hdl.handle.net/2433/135383.

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29

Collette, Nicole Marie. "Characterization of obesity in oMt1a-oGH transgenic mice /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2004. http://uclibs.org/PID/11984.

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30

Page, Raymond Lynn. "Evaluation of techniques for the production of transgenic animals." Diss., Virginia Tech, 1993. http://hdl.handle.net/10919/40112.

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31

Page, Raymond L. "Evaluation of techniques for the production of transgenic animals." Diss., Virginia Tech, 1993. http://hdl.handle.net/10919/40112.

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A polymerase chain reaction (PCR) technique was used to detect transgene presence after pronuclear microinjection of mouse zygotes cultured to various stages of development. The transgene was detected in 88% of 1-cell, 88% of 2-cell, 44% of 4-cell, 40% of morula, and 29% of blastocysts. By comparison, the integration frequency for transgenic mice made using the same DNA construct was 22%. After 5 days of in vitro culture, the injected construct was detected in 83% of arrested 1-cell, 85% of arrested 2-cell, and 85% of fragmented embryos. Only 28% of zygotes cultured after microinjection of DNA developed to the blastocyst stage compared to 74% of noninjected zygotes. When DNA buffer alone was injected, 63% of zygotes developed to the blastocyst stage. These data suggest that pronuclear microinjection of DNA is highly detrimental to subsequent embryonic development. Also, most injected DNA that is either unintegrated or that will not be integrated into the genome has been degraded by the blastocyst stage such that it can no longer be detected by PCR. The production of transgenic mice by cytoplasmic injection of DNA mixed with poly-L-lysine is also described. The effects of DNA concentration and stoichiometric ratio of positive charges provided by the polycation to negative charges provided by DNA on transgenic frequency and embryonic viability were studied. The highest transgenic frequency (13% of pups born were transgenic) was obtained when a polylysine/DNA complex having a stoichiometric charge ratio of one to one (equal positive charges as negative charges) at a DNA concentration of 50 ug/ml was used. The transgenic frequency by pronuclear injection of the same DNA construct was 22%. The percentage of zygotes, cultured in vitro, reaching the blastocyst stage which were injected cytoplasmicly was not different (p>0.05) than that of control zygotes that were not microinjected (65% versus 74%, respectively). The percentage of zygotes reaching the blastocyst stage after pronuclear microinjection with DNA at a concentration of 1.5 ug/ml was significantly lower (p<0.05) than control embryos (28% versus 74%, respectively). The overall transgenic pup production efficiency (percent of transgenic pups per embryos transferred) by cytoplasmic injection was 2.4% compared to 3.5% by pronuclear microinjection.<br>Ph. D.
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32

Chung, Chi-kin Samuel. "The development and characterization of a gene-knockout mouse model for secretin receptor /." View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31491121.

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33

Yang, Xiu. "Altered neuronal lineages in the facial ganglia of Hoxa₂ mutant mice." Cleveland, Ohio : Case Western Reserve University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1207189742.

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34

陳醒覺 and Sing-kwok Chan. "Mouse preproendothelin-1 gene: transgenic mouse models to study tissue-specific and developmental expression andregulation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31236571.

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35

Rojas, José-Manuel. "Identification of novel immunogenic HLA-DR-restricted peptides from tumour-associated antigens." Thesis, Nottingham Trent University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273771.

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CD4+ T cells playa central role in antitumour immunity; not only do they provide help for the development of CTL recognising tumour antigens but they can also enhance antitumour responses via indirect cytotoxic mechanisms at the tumour site. Since CD4+ T cells recognise the antigen in the form of pep tides presented on MHC class II molecules, attention has been focused in the recent years on the identification of these peptides derived from tumour antigens. Therefore the aim of this study was to identify novel immunogenic peptides derived from tumour antigens where presentation was restricted to human MHC class II HLA-DRI and/or HLADR4 molecules. The adopted strategy consisted in predicting peptides from the tumour antigens p53, gplOO and bcr-abl(b3a2) using computer-assisted algorithms, and immunisation of HLA-DRI transgenic mice with these peptides in order to assess their immunogenicity. Immunogenic peptides in transgenic mice were then tested in human in in vitro T cell sensitisation assays. To determine peptide immunogenicity in mice, a method was optimised using the reported I-Ak-restricted peptides HEL46-61 and HEL1l 9-132. This model was then successfully established in HLA-DRI transgenic mice with the model peptide HA307- 319. Proliferative responses and IFN-y production were observed when the splenocytes of HLA-DRI transgenic mice were re-presented in vitro with the HA307-319 peptide used in immunisation. Dendritic cells (DC) were shown to be better antigen presenting cells (APC) than syngeneic splenocytes in proliferation assays; thus DC were subsequently used as APC in the all experiments. Further characterisation of DC, generated from bone marrow precursors by culture with GM-CSF, demonstrated that day 8 non-adherent cells matured with LPS were optimal for antigen presentation in this experimental setting. Immunisation of HLA-DRI transgenic mice with predicted peptides from p53, gplOO and bcr-abI(b3a2) resulted in HLA-DRlrestricted responses for two novel p53 peptides (p5363-77 and p53108-122) and two bcrabl peptides (bcr-abIGFK11 and bcr-abIATG1 8). Responses were also observed to two novel gp 100 peptides (gp 1 00194-208 and gp 100566-580). This study demonstrated that HLA-DR-restricted responses to novel peptides can be obtained in HLA-DRI transgenic mice. Furthermore, proliferative responses to p5363-77 in a HLA-DRI + donor, to gpl00566-580 in another HLA-DRl+ donor. and to p53108-122 in two HLA- -1- Abstract DR4+ donors demonstrated that these peptides were also immunogenic in human assays. Collectively, these results indicated that peptide immunisation of HLA-DRI transgenic mice could facilitate the identification of novel immunogenic HLA-DRrestricted pep tides from tumour antigens, that allow us to understand further the role of CD4+ in antitumour immunity and improve cancer immunotherapeutic strategies.
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36

Gilder, Michael Frederick James. "Molecular investigations in animal models of Huntington's disease." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325046.

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37

Siu, Kwan-yin. "The development and characterization of a knockout model for secretin." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40887674.

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38

Chan, Sing-kwok. "Mouse preproendothelin-1 gene : transgenic mouse models to study tissue-specific and developmental expression and regulation /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19737002.

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39

Lee, Yin-ting. "Molecular characterization of the insertional mouse mutant yellow submarine, Ysb /." Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B24709372.

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40

Canseco-Sedano, Rodolfo. "Factors affecting the efficiency of gene transfer in mice." Diss., This resource online, 1992. http://scholar.lib.vt.edu/theses/available/etd-03172010-020810/.

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41

Wood, Stephen Andrew. "V-myc expressing transgenic mice generated by recombinant retroviral infection." Thesis, The University of Sydney, 1990. https://hdl.handle.net/2123/26388.

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Recombinant retroviruses which express the v-myc oncogene from an internal major histocompatibility class I gene, H2Kb, promoter were used to generate transgenic mice by infection of preimplantation mouse embryos. Expression of the transgene was achieved in a range of cell types including lymphoid cells and was associated with the development of lymphomas in some of these mice. V-myc expression in heart, skeletal muscle, lung, kidney and brain, however, was not associated with the transformation of these other tissues. Prior to the production of the transgenic mice, however, a series of recombinant retroviruses needed to be constructed and analysed to determine the retrovirus most suited to infect the embryos. Two series of recombinant retroviruses were generated which differed by the amount of gag sequence retained in the retroviral vector on which they were based. The retention of extensive gag sequences resulted in the production of a higher viral tiers which enabled the infection of the preimplantation embryos. In both series of recombinant retroviruses the promoters in the viral LTRs and the internal H2Kb promoter were active in embryonic fibroblast cell lines. Coculture of preimplantation embryos with the recombinant retroviruses LHV or LHX resulted in three mice which had integrated the HV virus and one with LHX. This represented an overall infection success rate of 1% which was much lower than the 20% or greater anticipated. This low success was attributed to either the strain of mouse used in these experiments or viral receptor site competition by virions with non-integratable subgenomic RNA.
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42

Groom, Joanna Ruth School of Medicine UNSW. "Loss of immune regulatory checkpoints in BAFF transgenic mice." Awarded by:University of New South Wales. School of Medicine, 2006. http://handle.unsw.edu.au/1959.4/27281.

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Multiple checkpoints control the survival and activation of auto-reactive B cells. The discovery of the TNF family cytokine BAFF has been crucial to understanding peripheral B cell tolerance mechanisms. Homeostatic levels of BAFF are tightly regulated to maintain tolerance in the periphery. Chronically increased levels of BAFF lead to the survival of autoreactive B cells. Autoimmune patients display elevated serum BAFF levels. BAFF Tg mice model this situation with systemically high levels of BAFF and the subsequent development of two separate but related autoimmune syndromes; systemic lupus erythematosus (SLE) and Sj??gren???s syndrome (SS). The work conducted in this thesis further investigates the defects in tolerance down-stream of self-reactive B cell survival, which may contribute to autoimmune disease development in BAFF Tg mice. Expansion of the Marginal zone (MZ) B cell population correlates with the pathogenesis of several models of autoimmune disease. BAFF Tg mice are unique in that they not only display an increased splenic MZ B cell population, but also MZ B cells are found in the salivary glands of mice developing SS. The examination of genes differentially regulated between MZ and Follicular (Fo) B cells led to the investigation of sphingosine-1-phosphate receptor biology. The expression of S1P receptors was shown to be required for the positioning of MZ B cells in the spleen. Chronic BAFF stimulation alters the retention of MZ B cells through the alteration of S1P receptors and decreased integrin activation. The alteration of S1P receptors and increased ligand sensitivity leads to the accumulation of MZ B cells in the inflamed salivary glands of BAFF Tg mice. This works provides a potential mechanism for the tissue specificity seen in systemic autoimmune disease. The provision of T cell help to auto-reactive B cells is thought to underlie the development of SLE. BAFF Tg mice deficient in T cells surprisingly developed an SLE-like disease indistinguishable from that of BAFF Tg mice. Autoimmunity in BAFF Tg mice did however require signals through the toll-like receptor (TLR)-associated signalling adaptor, MyD88, which controlled the production of pathogenic autoantibodies. Therefore, autoimmunity in BAFF Tg mice results from altered B cell tolerance, which requires TLR signalling and is independent of T cell help. It is likely that autoimmune patients with elevated levels of BAFF show a similar basis for disease.
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Zhu, Lei 1980. "Perturbed B cell development in young B7.2 transgenic mice." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84090.

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The best-characterized costimulation system for naive T cell activation is the interaction between CD28 and B7.1 or B7.2 ligands expressed on antigen-presenting cells such as activated B cells. Unexpectedly, transgenic mice with constitutive expression of B7.2 on B lymphocytes do not develop systemic autoimmune diseases, but rather exhibit a reduction of the B cell compartment that involves a defect in B cell maturation occurring very early in the ontogeny. In this study, we show that the early B cell loss is accompanied by splenomegaly and lymphoadenopathy that are due to a dramatic and transient increase in eosinophils. This immune response leads to disturbed splenic architecture, and is mediated by CD4+ T cells. In the absence of CD4+ T cells, early B cell maturation is nevertheless perturbed. Thus, our findings indicate that both T cell subsets participate in the elimination of B cells, but through different mechanisms.
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44

Mao, Jian-Hua. "Stochastic modelling of tumorigenesis in p53 deficient transgenic mice." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286124.

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45

Thomas, Thomas David Colin. "Immunoregulation in the NOD mouse and NOD transgenic mice." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612992.

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46

Kim, Youngwoo. "Generation of transgenic mice for conditional overexpression of Sox9." Kyoto University, 2013. http://hdl.handle.net/2433/174810.

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47

Spratt, Christopher. "Development of behavioural tasks for phenotyping of transgenic mice." Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/23201.

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48

Costa, Vivian. "Effects of overexpressing ASIC2a and ASIC3 in transgenic mice." Diss., University of Iowa, 2009. https://ir.uiowa.edu/etd/1132.

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Acid-sensing ion channels (ASICs) are proton-gated cation channels expressed throughout the nervous system. These channels are activated by acidic pH conditions within an attainable physiologic range. The specific function of these channels has proven to be elusive, but it is clear that they are involved in various neuronal processes, both in the central nervous system as well as in the periphery.In order to further study the functions of these channels in an animal model system, transgenic animals were generated that overexpress individual ASIC subunits: ASIC2a and ASIC3. Transgenic proteins were detectable in brain and peripheral nervous tissue, and each had differential effects on acid-gated current properties in cultured neurons.Transgenes included N-terminal epitope tags to distinguish from endogenous ASICs, and expression was driven by a pan-neuronal promoter. Mechanical thermal sensory behaviors were tested in the transgenic mice. However, no effect was observed in these behaviors. The most interesting effect of overexpressing ASIC3 was the resulting impairment of conditioned fear behaviors in the transgenic animals without effect on unconditioned fear. ASIC3 transgenic behave like ASIC1a knockout mice in conditioned fear behaviors. Transgenic ASIC3 interacts with endogenous ASIC1, and is likely altering subunit composition of ASIC channels in the brain without abolishing proton-gated currenst like in the ASIC1a knockout. Overexpressing these two ASIC subunits in transgenic animals has produced tools that may be used to further study the functions of these channels. While this still is an artificial setting for studying ASIC functions, it nonetheless provides an in vivo method to study the effects of altering subunit composition in a whole animal and its behavioral effects, as well as in vivo expression of transgenes that can be studies biochemically. It is hopeful that studying localization in the transgenic mice will afford a better understanding of the localization and function of endogenous channels without the limitations of generating antibodies against endogenous mouse ASIC proteins, which is still in progress.
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Kashinathrao, Mamta. "Recurrent genetic alterations in thymic lymphomas of LckMyrAkt2 transgenic mice." Click here for download, 2006. http://wwwlib.umi.com/cr/villanova/fullcit?p1432499.

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凌錦榮 and Kam-wing Ling. "Study of transgenic mice ectopically expressing the mouse Hoxb-3 gene." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31238993.

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