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Dissertations / Theses on the topic 'Juan de Celis'

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Published: 2 June 2025

Last updated: 31 July 2025

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1

Jun, SangMu. "Vaccine platform for infection or autoimmune diseases using an ETEC fimbrial scaffold." Diss., Montana State University, 2009. http://etd.lib.montana.edu/etd/2009/jun/JunS0509.pdf.

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2

Du, Juan [Verfasser]. "Electrochemical deposition of dye-modified ZnO hybrid thin films and their application to flexible dye-sensitized solar cells / Juan Du." Hannover : Technische Informationsbibliothek und Universitätsbibliothek Hannover (TIB), 2013. http://d-nb.info/1032724811/34.

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3

SILVA, FLAVIO S. "Clonagem, expressão, purificação e caracterização estrutural da região AP-1 da oncoproteína Jun." reponame:Repositório Institucional do IPEN, 2014. http://repositorio.ipen.br:8080/xmlui/handle/123456789/11802.

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Submitted by Claudinei Pracidelli (cpracide@ipen.br) on 2014-11-10T11:41:14Z No. of bitstreams: 0<br>Made available in DSpace on 2014-11-10T11:41:14Z (GMT). No. of bitstreams: 0<br>Dissertação (Mestrado em Tecnologia Nuclear)<br>IPEN/D<br>Instituto de Pesquisas Energeticas e Nucleares - IPEN-CNEN/SP

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4

Ramo, Kasmir. "Jun Kinases in Hematopoiesis, and Vascular Development and Function: A Dissertation." eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/789.

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Arterial occlusive diseases are major causes of morbidity and mortality in industrialized countries and represent a huge economic burden. The extent of the native collateral circulation is an important determinant of blood perfusion restoration and therefore the severity of tissue damage and functional impairment that ensues following arterial occlusion. Understanding the mechanisms responsible for collateral artery development may provide avenues for therapeutic intervention. Here, we identify a critical requirement for mixed lineage kinase (MLK) – cJun-NH2-terminal kinase (JNK) signaling in

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5

Peng, Jun [Verfasser]. "Effect of mesenchymal stem cells on coxsackievirus B3-induced inflammatory cardiomyopathy / Jun Peng." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2010. http://d-nb.info/1024365638/34.

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6

Allanson, Judith. "The role of protooncogene c-jun in differentiation and survival of neuronal cells." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285449.

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7

Chaudhury, Hera Ashraf. "c-Jun N-terminal kinase primes endothelial cells at atheroprone sites for apoptosis." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/6136.

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Atherosclerosis can be initiated by pro-inflammatory activation of endothelial cells (EC) which leads to the recruitment of leukocytes to the vessel wall, and also by endothelial apoptosis which elevates the permeability of arteries to lipoproteins. The greater curvature of the aorta is exposed to high shear and is protected from EC apoptosis, inflammation and atherosclerosis, whereas the lesser curvature is exposed to low shear and is susceptible to atherosclerosis. Pro-inflammatory mediators (e.g. TNFα, LPS) trigger phosphorylation of c-Jun N-terminal kinase (JNK) and p38 MAP kinases to posi

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8

Tomc, Lyn Kathryn. "Role of MEF2 proteins in the activation of the c-jun and MCK genes in skeletal muscle /." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0018/MQ56210.pdf.

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9

Sonuc, Niluefer. "C- jun downregulation sensitizes hepatoma cells to receptor induced apoptosis through preventing FADD phosphorylation." Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-106724.

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10

VanDyke, Jamie E. "Modeling laser effects on multi-junction solar cells using Silvaco ATLAS software for spacecraft power beaming applications." Thesis, Monterey, California : Naval Postgraduate School, 2010. http://edocs.nps.edu/npspubs/scholarly/theses/2010/Jun/10Jun%5FVanDyke.pdf.

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Thesis (M.S. in Space Systems Operations)--Naval Postgraduate School, June 2010.<br>Thesis Advisor(s): Michael, Sherif ; Second Reader: Scott, Alan. "June 2010." Description based on title screen as viewed on July 14, 2010. Author(s) subject terms: Solar Cell, Photovoltaic, Directed Energy, Power Beaming, Wireless Power Transfer, Multi-junction, Laser, Silvaco, Modeling, Simulation. Includes bibliographical references (p. 115-117). Also available in print.

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11

Maaske, André Juan [Verfasser], Matthias [Gutachter] Tenbusch, and Raphael [Gutachter] Stoll. "Treatment of allergic asthma by gene based immunizations that induce specific targeting of antigens toward dendritic cells / André Juan Maaske ; Gutachter: Matthias Tenbusch, Raphael Stoll." Bochum : Ruhr-Universität Bochum, 2017. http://d-nb.info/1129452441/34.

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12

Peer, Zada Abdul Ali. "Signaling through CD44 affects cell cycle progression and c-Jun expression in acute myeloid leukemia cells." Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-28659.

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13

Ueno, Yasushi. "Lysophosphatidylcholine phosphorylates CREB and activates the jun2TRE site of c-jun promoter in vascular endothelial cells." Kyoto University, 2002. http://hdl.handle.net/2433/149723.

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14

Lu, Qiang, and 呂強. "The effects of CNTF and BDNF on c-jun expression, survival and regeneration of axotomized retinal ganglion cells in adult goldenhamsters." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31240689.

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15

Yuzuriha, Akinori. "Extracellular laminin regulates hematopoietic potential of pluripotent stem cells through integrin β1-ILK-β-catenin-JUN axis". Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/264664.

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16

Acien, Caroline. "Rôle du facteur de transcription c-Jun dans l'ontogénie et l'homéostasie des macrophages." Thesis, Aix-Marseille, 2014. http://www.theses.fr/2014AIXM4010.

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Pour étudier le rôle de c-Jun dans les macrophages, nous avons développé deux modèles murins présentant une délétion spécifique de Jun dans la lignée de cellules myéloïdes. Le 1er modèle (JunΔCsf1r) a une délétion de c-Jun dans les cellules myéloïdes et leurs progéniteurs. Le 2nd modèle (JunΔLyz2) a une perte de c-Jun dans les cellules myéloïdes matures. L'analyse de ces modèles a montré que l'expression de c-Jun n'est pas nécessaire à l'homéostasie des macrophages tissulaires, mais est essentiel à l'expansion des macrophages de la MO et des progéniteurs de la rate. De plus, l'absence d'expres

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17

Wang, Fang St George Clinical school UNSW. "Oxidative stress induced C-Jun N-terminal Kinase (JNK) activation in tendon cells upregulates MMP1 mRNA and protein expression." Awarded by:University of New South Wales. St George Clinical school, 2006. http://handle.unsw.edu.au/1959.4/28815.

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To explore the potential mechanisms of tendon degeneration, we investigated the role of c-Jun N-terminal Kinase (JNK) activation and the regulation of matrix metalloproteinase 1 (MMP1) in tendon matrix degradation under oxidative stress. JNK and MMP1 activity in samples from normal and ruptured human supraspinatus tendons were evaluated by immunohistochemistry. Real-time quantitative PCR was utilized to evaluate MMP1 mRNA expression and western blotting for MMP1 and JNK protein detection. JNK activation and increased MMP1 activity were found in the torn human supraspinatus tendon tissue, as we

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18

Hoeck, J. D. "The role of Fbw7 and its substrates Notch and c-Jun in neural stem cells, the brain and development." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1335829/.

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Activation of the oncogenic transcription factor c-Jun by the Jun N-terminal kinase (JNK) has been implicated in diverse biological effects, for example promoting intestinal proliferation or inducing neural apoptosis. Apart from differentiation, apoptosis plays an important role in the specification of neuronal networks in the developing brain. However, the molecular mechanisms governing differentiation and apoptosis during brain development are incompletely understood. In my PhD studies, I have shown for the first time that the E3 ubiquitin ligase substrate recognition component Fbw7 (F-box a

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19

Alkhoury, Kenan. "Mechanisms responsible for homocysteine mediated damage to human endothelial cells : the role of oxidative stress in atherogenesis." Thesis, University of Bradford, 2009. http://hdl.handle.net/10454/4300.

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Homocysteine (Hcy) has been identified as a primary risk factor for atherosclerosis as it induces endothelial cell (EC) activation/dysfunction and thus potentially initiating atherosclerotic plaque formation. There is accumulating evidence indicating a key role for oxidative stress in mediating Hcy atherogenic effects. The aim of this study was to evaluate the effects of chronic treatment with Hcy on EC activation and to explore the role of oxidative stress in these effects. Human umbilical vein endothelial cells (HUVEC) were cultured and treated chronically with DL-Hcy for 5-9 days. An in vit

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20

Gudey, Shyam Kumar. "TRAF6 stimulates TGFβ-induced oncogenic signal transduction in cancer cells". Doctoral thesis, Umeå universitet, Institutionen för medicinsk biovetenskap, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-87017.

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Prostate cancer is one of the leading causes of cancer-related deaths in men worldwide, with 10,000 new cases/year diagnosed in Sweden. In this context, there is an urgent need to identify new biomarkers to detect prostate cancer at an initial stage for earlier treatment intervention. Although how prostate cancer develops has not been fully established, the male sex hormone testosterone is a known prerequisite for prostate cancer development. High levels of transforming growth factor-β (TGFβ) are prognostically unfavorable in prostate cancer patients. TGFβ is a multifunctional cytokine that re

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21

Lepique, Ana Paula. "Efeitos de ACTH, PMA e dcAMP na expressão de genes das famílias FOS e JUN do gene C-MYC e na atividade do fator de transcrição AP-1 em células adrenocorticais Y-1." Universidade de São Paulo, 1996. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-18092008-093726/.

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As células Y-1 pertencem a uma linhagem clonal de células funcionais de córtex adrenal de camundongo, que respondem a ACTH. Em células Y-1, ACTH promove a esteroidogênese (função) e tem efeitos regulatórios complexos na transição G0→G1→S do ciclo celular. ACTH promove a transição G0→G1, mas inibe a transição G1→S. É possível que a regulação do ciclo celular por ACTH seja mediada pelo controle da expressão dos proto-oncogenes das famílias fos, jun e myc. Nosso laboratório mostrou, anteriormente, que ACTH induz a expressão dos genes fos e jun, mas inibe c-myc. O objetivo

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22

Hess, Patricia M. "Role of c-Jun NH-terminal Kinase in Bcr/Abl Induced Cell Transformation: a dissertation." eScholarship@UMMS, 2003. https://escholarship.umassmed.edu/gsbs_diss/88.

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The c-Jun NH2-terminal kinase (JNK) group of kinases include ten members that are created by alternative splicing of transcripts derived from Jnk1, Jnk2 and Jnk3 genes. The JNK1 and JNK2 protein kinases are ubiquitously expressed while JNK3 is expressed in a limited number of tissues. The JNK signaling pathway is implicated in multiple physiological processes including cell transformation. There is growing evidence that JNK signaling is involved in oncogenesis. Nevertheless, the role that JNK plays in malignant transformation is still unclear. The aim of this thesis is to examine the role of J

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23

MacDonald, Jennifer M. "A Role for c-Jun Kinase (JNK) Signaling in Glial Engulfment of Degenerating Axons: A Dissertation." eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/609.

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The central nervous system (CNS) is composed of two types of cells: neurons that send electrical signals to transmit information throughout the animal and glial cells. Glial cells were long thought to be merely support cells for the neurons; however, recent work has identified many critical roles for these cells during development and in the mature animal. In the CNS, glial cells act as the resident immune cell and they are responsible for the clearance of dead or dying material. After neuronal injury or death, glial cells become reactive, exhibiting dramatic changes in morphology and patterns

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24

Pernuš, Agata [Verfasser], and Jörg [Akademischer Betreuer] Langowski. "Imaging mobility and interaction of c-Fos and c-Jun transcription factors in live cells: A SPIM-FCCS study / Agata Pernus ; Betreuer: Jörg Langowski." Heidelberg : Universitätsbibliothek Heidelberg, 2015. http://d-nb.info/1180500849/34.

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25

Wang, Jun [Verfasser], and Birgit [Akademischer Betreuer] Schittek. "The regulatory mechanisms of enhancing IGF-1R expression and activity and the impact on therapy resistance of melanoma cells / Jun Wang ; Betreuer: Birgit Schittek." Tübingen : Universitätsbibliothek Tübingen, 2016. http://d-nb.info/1198122552/34.

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26

Braun, Julian [Verfasser], Andreas [Akademischer Betreuer] Thiel, Jun [Akademischer Betreuer] Dong, Leif-Andreas [Akademischer Betreuer] Garbe, and Andreas [Akademischer Betreuer] Kurtz. "Analysis of the derivation phase of human adipose tissue-derived multipotent mesenchymal stromal cells / Julian Braun. Gutachter: Leif-Andreas Garbe ; Andreas Kurtz. Betreuer: Andreas Thiel ; Jun Dong." Berlin : Technische Universität Berlin, 2013. http://d-nb.info/1065664672/34.

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27

Eynott, Paul Robert. "Modulation of eosinophilic inflammation, cellular proliferation & bronchial hyperresponsiveness following single and repeated allergen exposure by inhibitors of T-cells, nitric oxide synthase and Jun N-terminal kinase." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405015.

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28

Herbert, Brittney-Shea. "Mechanisms of RRR-[alpha]-tocopheryl succinate- and N-(4-hydroxyphenyl)retinamide-induced apoptosis of human HL-60 myelocytic leukemia and MDA-MB-435 breast cancer cells : a role for TGF-[beta] and C-JUN /." Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.

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29

Henrie, Hélène. "Régulation de la dynamique des microtubules par la kinase de stress JNK dans les cellules épithéliales : caractérisation de CLIP-170 comme un nouveau substrat." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS461/document.

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Les microtubules sont des éléments dynamiques du cytosquelette qui contrôlent à la fois l’organisation du cytoplasme, la polarité, la migration et la division cellulaire. Notre laboratoire a précédemment montré que la kinase de stress JNK (c-Jun NH2-terminal Kinase) régule la dynamique des microtubules dans les cellules épithéliales de mammifères, en augmentant les vitesses de polymérisation, ainsi que les fréquences de sauvetage (transition vers une phase de repolymérisation). Alors que certaines protéines neuronales capables de réguler la dynamique des microtubules ont été identifiées comme

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Amin, Shahreen. "Regulation of the tyrosine phosphatase SHP-1 expression by C-jun-N-terminal kinase and RFX-1 and AP-4 transcription factors in insulin-like growth factor-1 (IGF-1) stimulated breast adenocarcinoma MCF-7 cells." Thesis, University of Ottawa (Canada), 2005. http://hdl.handle.net/10393/26837.

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This thesis is devoted to reveal the negative regulators in IGF-1 (Insulin like growth factor 1) stimulated growth of a human breast adenocarcinoma cell line. It is a well established fact that increased circulating levels of IGF-1 correlate with increased risk of breast cancer. IGF-1 activation of its receptor, IGF-1R, is implicated in the progression of breast cancer, where IGF-1 stimulation leads to proliferative and anti-apoptotic responses by stimulating MAPK Erk and PI3K, respectively. In this study, IGF-1 stimulated MCF-7 cells proliferated more in the absence of MAPK JNK, implicating t

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Zamani, Marzieh. "The role of the JNK/AP-1 pathway in the induction of iNOS and CATs in vascular cells." Thesis, University of Hertfordshire, 2013. http://hdl.handle.net/2299/10626.

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Nitric oxide (NO) is an important biological molecule within the body, which over production of this molecule in response to different stimulations can cause various inflammatory diseases. Over production of this molecule is caused by the induction of the inducible nitric oxide synthase (iNOS) enzyme. This enzyme uses L-arginine as a substrate and therefore the presence and transport of this amino acid into the cells can be a key factor in regulating NO over production. Different signalling mechanisms have been implicated in the regulation of this pathway and one of which involves the Mitogen

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Tesz, Gregory J. "Role of MAP4K4 Signaling in Adipocyte and Macrophage Derived Inflammation: A Dissertation." eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/380.

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Human obesity is increasing globally at an impressive rate. The rise in obesity has led to an increase in diseases associated with obesity, such as type 2 diabetes. A major prerequisite for this disease is the development of insulin resistance in the muscle and adipose tissues. Interestingly, experiments in rodent models suggest that adipocytes and macrophages can profoundly influence the development of insulin resistance. Accordingly, the number of adipose tissue macrophages increases substantially during the development of obesity. Numerous research models have demonstrated that macrophages

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Aguilar, Pimentel Juan Antonio [Verfasser]. "Role of allergen-specific CD8+ T cells in the murine asthma model / Juan Antonio Aguilar Pimentel." 2010. http://d-nb.info/101091359X/34.

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34

Tzu-Ching, Meng, and 孟子青. "Intracellular components regulate c-jun gene expression during MMS treatment in NIH3T3 cells." Thesis, 1994. http://ndltd.ncl.edu.tw/handle/37851586869366903158.

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碩士<br>國立臺灣大學<br>毒理學研究所<br>82<br>Exposure of NIH3T3 cells with alkylating agent methyl methane- sulfonate(MMS) leads to the transient induction of c-jun gene. Several lines of evidence have shown that the activation of protein kinases can accelerate c-jun mRNA transcription, but our result clearly demonstrated that pretreatment with different kinase inhibitors did not alter the MMS-induced c-jun transcript expression.When both parental NIH3T3 cells and v-Ha- ras transformed NIH3T3 cells are

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Lo, Chia-Yu, and 羅嘉瑜. "Histone Deacetylase Inhibitors Attenuate c-Jun Expression Induced by Epidermal Growth Factor in A431 Cells." Thesis, 2002. http://ndltd.ncl.edu.tw/handle/17165425039163097331.

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碩士<br>國立成功大學<br>藥理學研究所<br>90<br>Eukayotic transcription is a highly regulated process, and histone acetylation is now known to play a major role in this regulation. Acetylation of histone N-termini reduces chromatin condensation; thus gene transcription may activate. Previously, we found that c-Jun induction was required in epidermal growth factor (EGF) induced human 12(S)-lipoxygenase (12(S)-LOX) gene expression in human epidermoid carcinoma A431 cells. In this study, we studied the effect of histone deacetylase inhibitors, trichostatin A (TSA) and sodium butyrate (NaBT) on EGF induced exp

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Melino, Michelle. "The role of c-jun N-terminal kinase (JNK) in human T cell function." Thesis, 2009. http://hdl.handle.net/2440/56209.

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T cells are involved in cellular pathways which enable the immune system to protect us against infection and cancer. However, the same mechanisms also allow T cells to generate chronic inflammatory conditions, including autoimmunity and allergy. Thus a concerted effort has been made to try to understand how the immune system functions in order to inhibit responses which may have harmful effects on tissues and organs. There is a continued search for new immunosuppressants which can only be accomplished through a better understanding of the pathways that regulate T cell function. This includes

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Melino, Michelle. "The role of c-jun N-terminal kinase (JNK) in human T cell function." 2009. http://hdl.handle.net/2440/56209.

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T cells are involved in cellular pathways which enable the immune system to protect us against infection and cancer. However, the same mechanisms also allow T cells to generate chronic inflammatory conditions, including autoimmunity and allergy. Thus a concerted effort has been made to try to understand how the immune system functions in order to inhibit responses which may have harmful effects on tissues and organs. There is a continued search for new immunosuppressants which can only be accomplished through a better understanding of the pathways that regulate T cell function. This includes t

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Huang, Shu-Yu, and 黃淑于. "Effects of Apigenin on TPA induced c-jun and c-fos Protooncogene Expression in NIH3T3 Cells." Thesis, 1993. http://ndltd.ncl.edu.tw/handle/99969378046532572290.

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碩士<br>國立臺灣大學<br>毒理學研究所<br>81<br>Apigenin, a plant flavonoid, could interfere TPA induced tumor promoting phenomena in NIH3T3 cells, such as c-jun and c- fos gene expression, 80kDa protein phosphorylation, lipid per- oxidation and cell proliferation. In our study, TPA induced c- fos gene expression in NIH3T3 cells suppressed by 10, 50, or 100mM of apigenin. On the other hand, TPA activated c-jun gene expression also suppressed by apigenin. At 10mM of apigenin, c- jun mRNA production repres

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Yen-Chen, Hu, and 胡燕真. "Low substratum rigidity induces ubiquitin ligase Cul1 mediated-c-Jun degradation in nucleus of epithelial cells." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/71278981631236278819.

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碩士<br>國立成功大學<br>生理學研究所<br>94<br>Abstract The proto-oncoprotein c-Jun is a component of the transcription factor AP-1 (activator protein-1) involved in cellular proliferation, differentiation and death. Maintenance of c-Jun protein levels plays an important role in proliferation and survival of epithelial cells. Previous studies in our lab showed that epithelial cells cultured on collagen gel developed apoptosis due to low substratum rigidity. Low rigidity-induced cell apoptosis was mediated by degradation of c-Jun, which was observed only in epithelial, but not transformed cells. The purpose o

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Chen, Yun-Ju, and 陳韻如. "Involvement of protein dephosphorylation in EGF-induced interaction between c-Jun and Sp1 in A431 cells." Thesis, 2003. http://ndltd.ncl.edu.tw/handle/30201053439867460466.

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碩士<br>國立成功大學<br>藥理學研究所<br>92<br>It is reported that modification of transcriptional factor is important for gene regulation. In recent years, we have found that EGF induces 12(S)-lipoxygenase gene expression via activation of Ras-Rac-JNK and Ras-ERK pathways in A431 cells, and also increases c-Jun biosynthesis. Furthermore, We found that 12(S)-lipoxygenase promoter without AP1 consensus binding site is induced by c-Jun overexpression, and the c-Jun/Sp1 interaction plays an important role in EGF-induced 12(S)-lipoxygenase gene expression. Therefore, we are interested in studying the regulation

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LI, HENG, and 李珩. "The effects of glucocorticoid hormone on the expression of c-jun in NIH 3 T3 cells." Thesis, 1987. http://ndltd.ncl.edu.tw/handle/51614882694322765645.

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42

Sonuc, Nilüfer [Verfasser]. "C-jun downregulation sensitizes hepatoma cells to receptor induced apoptosis through preventing FADD phosphorylation / by Nilüfer Sonuc." 2008. http://d-nb.info/998366927/34.

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Yao, Jeng Yuan, and 姚政源. "TAp63 is regulated by c-jun and plays compensatory roles in p53-deficient cancer cells under genotoxic stress." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/54657198423890906607.

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博士<br>長庚大學<br>生物醫學研究所<br>99<br>The transcription factor p63 belongs to the p53 protein family and plays an important role in epithelial development. Recent studies showed that p63 is over-expressed in some human squamous cell carcinomas of the head and neck, suggesting a role in carcinogenesis. The p63 gene contains two promoters and alternative promoter usage generates two groups of proteins with (TAp63) or without (ΔNp63) the transactivation domain. Although the roles of TAp63 in epithelial development have been described in numerous recent studies, the regulation of its expression has not b

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Chen, Shu-Ting, and 陳淑婷. "ARNT cooperates with c-Jun/Sp1 to regulate EGF-induced 12(S)-lipoxygenase gene expression in A431 cells." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/16604875801440074542.

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碩士<br>國立成功大學<br>藥理學研究所<br>95<br>It is well documented that EGF regulates the gene expression including 12(S)-lipoxygenase and p21WAF1/CIP1 through the transcription factor c-Jun and Sp1. However, the signaling molecules involved in EGF-responsive gene expression are not totally calified. Here we used the immunoprecipitation and followed by MALDI-TOF to analyze Sp1-associated proteins. We found that ARNT, a hypoxia related transcription factor, co-immunoprecipitated with Sp1. This result suggested that ARNT may play a role in EGF signaling event under physicial condiction. We found that EGF sti

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Lin, Bor-tyng, and 林伯庭. "The Role of c-Jun N-terminal Kinase in Angiotensin II-induced Cellular Senescence of Vascular Smooth Muscle Cells." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/10684685523838938535.

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碩士<br>國立成功大學<br>細胞生物及解剖學研究所<br>96<br>Abdominal aortic aneurysm (AAA) is present in 8% of the population over 60 years of age and exhibits a high mortality rate when rupture. AAA is characterized by extracellular matrix destruction and depletion of vascular smooth muscle cells (VSMC) in the tunica media. Angiotensin II (Ang II) was shown to induce AAA formation in animal models and c-Jun N-terminal kinase (JNK) was shown to play a critical role. A previous study suggested that Ang II induces premature senescence of VSMCs via a p53/p21-dependent pathway. We hypothesized that JNK activation media

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JIANG, MING-CONG, and 江明聰. "Induction of c-fos and c-jun mRNAs accumulation by muscarinic acetylcholine receptor M5 in transfected murine L cells." Thesis, 1991. http://ndltd.ncl.edu.tw/handle/54236043237947016119.

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Hung, Pei-Shan, and 洪珮珊. "Ovatodiolide induces apoptosis through reactive oxygen species-activated ATM and JNK/c-Jun signaling pathway in human lung cancer cells." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/34472076895972775408.

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碩士<br>國立中興大學<br>生命科學系所<br>103<br>The statistic documents from Ministry of Health and Welfare indicate that lung cancer is the first leading cause of cancer mortality in Taiwan, and increased gradually nowadays. Smoking, air pollution and soot are the high risk factors of lung cancer. Surgery, chemotherapy, radiation therapy and targeted therapy are the common treatments for lung cancer patients. However, the curing rate of these patients is still limited, to develop the safe and effective therapeutic strategy or agent is urgently needed. Previous studies have shown that inhibition of cell grow

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Tzeng, Tzi-Fei, and 曾姿斐. "Involvement of reactive oxygen species/c-Jun NH2-terminal kinase pathway in Kotomolide A induces apoptosis in human breast cancer cells." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/96259042497098664945.

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碩士<br>高雄醫學大學<br>天然藥物研究所<br>96<br>The anticancer effects of kotomolide A (KTA), a new butanolide constituent isolated from the leaves of Cinnamomum kotoense (Lauraceae), on the two human breast cancer cell lines MCF-7 and MDA-MB-231, were first investigated in our study. KTA exhibited selectively antiproliferative effects in cancer cell lines without showing any toxicity in normal mammary epithelial cells. Treatment of cancer cells with KTA to trigger G2/M phase arrest was associated with increased p21/WAF1 levels and reduced amounts of cyclin A, cyclin B1, cdc2 and cdc25C. KTA induced cancer c

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Wang, Hsiu-Yun, and 王綉雲. "Effect of phospholipid hydroperoxide glutathione peroxidase (PHGPx) on expression of c-Jun inducing by EGF in human epidermoid carcinoma A431 cells." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/92180750879246517939.

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碩士<br>中華醫事科技大學<br>生物科技研究所<br>95<br>Reactive oxygen species (ROS) are highly oxidative molecules and may be induced by intracellular or extracellular elements. Recent evidence suggests that ROS may play an important role in cell signal transduction, such as MAPKs which including ERK, JNK and p38 signal pathways. In antioxidant enzymes, phospholipid hydroperoxide glutathione peroxidase (PHGPx) can directly protect cell membrane from the damage of oxidative stress. Additional, PHGPx contains strongly ability of antioxidation and may participate in regulation of signal transduction. Previously, we

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Peer, Zada Abdul Ali [Verfasser]. "Signaling through CD44 affects cell cycle progression and c-Jun expression in acute myeloid leukemia cells / vorgelegt von Abdul Ali Peer Zada." 2004. http://d-nb.info/973138475/34.

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