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Dissertations / Theses on the topic 'Inhibiteurs de JAK/STAT'

Author: Grafiati
Published: 22 June 2024
Last updated: 31 July 2025

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1

Jeanpierre, Marie. "Implication de la voie de signalisation JAK/STAT dans le développement de maladies auto-immunes : caractérisation de maladies monogéniques et identification de cibles thérapeutiques." Electronic Thesis or Diss., Université Paris Cité, 2025. http://www.theses.fr/2025UNIP5007.

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La voie de signalisation JAK/STAT est au coeur de la transduction de nombreuses cytokines, elle est finement régulée par des inhibiteurs afin d'empêcher un emballement des réponses cytokiniques. C'est une voie essentielle pour l'orchestration du système immunitaire, souligné par le nombre croissant de variants caractérisés dans un large spectre de maladies, allant de l'immuno-déficience à l'auto-immunité et aux cancers. Dans le laboratoire d'accueil, nous utilisons le modèle unique que sont les maladies monogéniques afin d'appréhender les mécanismes physiopathologiques menant à la dérégulation
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2

Guégan, Nicolas. "Étude du rôle des mutations de la voie JAK-STAT dans la lymphomagenèse associée à la maladie cœliaque." Electronic Thesis or Diss., Université Paris Cité, 2024. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=6776&f=79039.

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La maladie cœliaque réfractaire de type 2 (MCR2) est un lymphome intraépithélial de bas grade compliquant la maladie cœliaque (MC), et une première étape fréquente vers un lymphome invasif, le lymphome T associé à une entéropathie (EATL). Les cellules de MCR2 sont issues d'une petite sous-population de lymphocytes intraépithéliaux (LIE) appelée LIE iCD3+ innés, présents dans l'intestin normal. Ces cellules, dépourvues de CD3 à leur surface (sCD3-), combinent des caractéristiques de cellules T et NK et se différencient dans l'intestin à partir d'un précurseur hématopoïétique en réponse à un sig
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3

Berrabah, Sofia. "Etude de nouvelles cibles thérapeutiques dans les lymphomes compliquant la maladie cœliaque." Electronic Thesis or Diss., Université Paris Cité, 2021. http://www.theses.fr/2021UNIP5201.

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La maladie cœliaque réfractaire de type II (MCRII), autrement appelé lymphome intraépithélial, est une complication rare mais sévère de la maladie cœliaque caractérisée par une expansion clonale d'une population particulière de lymphocytes intraépithéliaux (LIE) innés, présents dans l'intestin normal chez l'Homme comme chez la souris. Notre laboratoire a montré que cette population particulière de LIE innés partage des caractéristiques communes à celles des lymphocytes T et des cellules NK. Ces « LIE iCD3+ innés » sont caractérisées par une expression de CD3 au niveau intracellulaire mais pas
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4

Jungalee, Anouchka. "Implication physiopathologique de l'adaptateur LNK : mécanismes d'action et perspectives thérapeutiques dans les Néoplasmes Myéloprolifératifs." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCD017/document.

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L’adaptateur LNK est un régulateur négatif des voies de signalisation, dont la voie JAK/STAT,essentielle au développement du système hématopoïétique. Son implication dans les hémopathies chroniques, notamment les Néoplasmes Myéloprolifératifs (NMP), a été mise en évidence par l’analyse de souris invalidées pour cet adaptateur et l’identification de mutations de LNK chez les patients atteints de ces pathologies. Toutefois, le mécanisme permettant la régulation de ses partenaires, dont la kinase JAK2, et l’implication fonctionnelle des mutations de LNK dans les NMP, restent à définir. Ainsi, mon
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5

Is'Harc, Hayaatun. "JAK/STAT signalling." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272414.

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6

Dawson, M. A. F. "JAK-STAT signalling at chromatin." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598423.

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The aim of my work was to explore the possibility that the mammalian JAK2 signalling pathway influences the structure and function of chromatin. I have demonstrated that JAK2 is present in the nucleus of both human haematopoietic cell lines and primary cells. My results suggest that JAK2 functions as a histone tyrosine kinase and phosphorylates histone H3 at tyrosine-41 (H3Y41). This novel histone modification, the first described tyrosine phosphorylation on any of the non-variant histones, regulates the binding of heterochromatin protein 1-alpha (HP1α) at a new binding site on chromatin. HP1α
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7

Broughton, Nicola Ann. "Specificity in JAK/STAT signal transduction." Thesis, King's College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300540.

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8

Zhu, Wei. "Negative regulation of JAK/STAT pathway /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2004. http://wwwlib.umi.com/cr/ucsd/fullcit?p3112843.

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9

Vogt, Katja L. "Endocytic regulation of JAK/STAT signalling." Thesis, University of Sheffield, 2014. http://etheses.whiterose.ac.uk/6655/.

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10

Moore, Rachel. "Regulation of JAK/STAT signalling by endocytosis." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/22459/.

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The JAK/STAT pathway is a highly evolutionarily conserved signal transduction pathway, whose activation can lead to a broad range of cellular outcomes. The pathway is used repeatedly during multiple developmental stages and in adult tissue, and therefore tight regulation is required to enable accurate responses in a context specific manner. Internalisation and endocytic trafficking of signalling components provides a mechanism whereby spatial compartmentalisation can enable distinct signalling outputs. Within this study I have investigated the role of endocytosis in the regulation of the Droso
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11

Leal, Cervantes Ana Irene. "Transcriptional consequences of Jak-Stat signalling in haematopoiesis." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709253.

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12

Röder, Sabine. "Signaltransduktion durch JAK-STAT-Moleküle bei der Polyzythämia vera." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972175741.

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13

Moubarak, Patricia. "Expression und Regulation von JAK/STAT-Proteinen im Pankreas." Diss., lmu, 2006. http://nbn-resolving.de/urn:nbn:de:bvb:19-53862.

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14

Pean, Claire. "JAK-STAT pathway in the control of mycobacterial infections." Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/jakstat-pathway-in-the-control-of-mycobacterial-infections(cb788a0d-1c53-4f5c-8513-64c8cb50e08e).html.

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Though mammalian JAKs and STATs have been extensively studied over the past 20 years, many aspects of their in vivo function remain unclear. In particular, their roles in control of infection with pathogens remain murky and confusing. One difficulty in understanding how these pathways regulate inflammation is the presence of complex compensatory mechanisms between the different JAK and STAT proteins. In the Dionne lab, we use the fruit-fly Drosophila melanogaster as a model to study the in vivo functions of the JAK/STAT pathway in mycobacterial infection. Flies contain only one JAK (hop), one
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15

Devergne, Olivier. "Étude de la voie JAK/STAT chez Drosophila melanogaster." Nice, 2006. http://www.theses.fr/2006NICE4030.

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Chez les mammifères, la voie de signalisation JAK/STAT est activée en réponse aux cytokines et aux facteurs de croissance. Son activation stimule la prolifération, la différentiation, la migration cellulaire ainsi que l'apoptose. Nous montrons que la voie JAK/STAT et son récepteur Domeless (Dome), un récepteur de la famille des récepteurs aux IL-6, sont requis pour la différenciation et la migration des cellules de la bordure, un modèle d'invasion cellulaire qui se déroule au cours de l'ovogenèse chez la drosophile. Nous nous sommes ensuite intéressés aux mécanismes impliqués dans le contrôle
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16

Chen, Qian. "THE INTERACTIONS BETWEEN JAK/STAT SIGNALING LIGANDS IN DROSOPHILA MELANOGASTER." UKnowledge, 2014. http://uknowledge.uky.edu/biology_etds/23.

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The development of multi-cellular organisms requires extensive cell-cell communication to coordinate cell functions. However, only a handful of signaling pathways have emerged to mediate all the intercellular communications; therefore, each of them is under an array of regulations to achieve signaling specificity and diversity. One such signaling pathway is the Janus Kinase/ Signal Transducer and Activator of Transcription (JAK/STAT) pathway, which is the primary signaling cascade responding to a variety of cytokines and growth factors in mammals and involved in many developmental processes. T
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17

Han, Ho-chun, and 韓浩俊. "JAK-STAT pathway as potential target of acute myeloid leukemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B50534208.

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 Acute myeloid leukemia (AML) is a group of heterogeneous diseases characterized by an abnormal increase in myeloblasts. Despite intensive chemotherapy and allogeneic bone marrow transplantation, the treatment outcome of AML remains unsatisfactory, with a cure rate of only about 30%. Therefore, novel therapeutic strategies targeting the pathogenetic pathways of leukemia initiation and progression are needed. Using intracellular phospho-flow analysis with normal bone marrow as reference, we detected an increase in phosphorylated-STAT5 (pSTAT5) in three leukemic cell lines (K562, KG-1 and ML-
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18

Stec, Wojciech. "Molecular analysis of the Drosophila JAK/STAT pathway receptor complex." Thesis, University of Sheffield, 2013. http://etheses.whiterose.ac.uk/4509/.

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The JAK/STAT signalling pathway plays a central role in numerous biological processes contributing to development and maintenance of homeostasis. Drosophila melanogaster offers a conserved JAK/STAT pathway with much lower redundancy. For this reason, the fruit fly was used as a model organism to investigate genetic interactions and functions of the JAK/STAT pathway in the context of the whole organism. However, very little is known regarding the molecular mechanisms governing the Drosophila JAK/STAT pathway. Here, we present a molecular analysis of the sole receptor of the JAK/STAT pathway in
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19

Thomas, Sally J. "Genetic and chemical modulators of JAK/STAT signalling in cancer." Thesis, University of Sheffield, 2015. http://etheses.whiterose.ac.uk/13230/.

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Activation of JAK/STAT signalling is a feature of many haematological malignancies and solid tumours. Better understanding of the molecular events contributing to JAK/STAT pathway activation, and a greater range of therapies acting on the pathway, should lead to improved treatment options for patients with malignancies associated with activation of the pathway. This work builds on screens that identified genes and drugs which modulate JAK/STAT signalling in the fruit fly Drosophila melanogaster, to determine whether these effects occur in the conserved human pathway. The gene ANKHD1 (Ankyrin R
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20

Kalymbetov, Anuar [Verfasser]. "Role of JAK/STAT signalling pathway in PAH / Anuar Kalymbetov." Gießen : Universitätsbibliothek, 2016. http://d-nb.info/1120270227/34.

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21

Giedt, Michelle Suzanne. "JAK/STAT SIGNALING REGULATES GAMETOGENESIS AND AGE-RELATED REPRODUCTIVE MAINTENANCE." UKnowledge, 2018. https://uknowledge.uky.edu/biology_etds/52.

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Cell signaling is central to integration of internal and external cues that regulate development and homeostasis. Most development is thought of as pre-adult, but limited developmental processes occur in adults. Gametogenesis incorporates elements of both these facets, with a distinct developmental plan for gamete synthesis which is regulated by integration of homeostatic inputs such as nutrient status, and environmental cues. Signaling pathways integrate and transduce information from these cues to evoke a response. A decline in homeostasis and subsequent cues occurs over time, in the case of
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22

Beirer, Stephan. "Mathematical modelling of the Jak-Stat1 signal transduction pathway." Berlin Logos, 2007. http://deposit.d-nb.de/cgi-bin/dokserv?id=2949679&prov=M&dok_var=1&dok_ext=htm.

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23

Litterst, Claudia Monika. "Untersuchungen zur Funktion von Koaktivatoren in der JAK-STAT-vermittelten Transkriptionsaktivierung." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=966005597.

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24

Park-Min, Kyung-Hyun. "The crosstalk between ITAM-associated receptors and Jak-STAT signaling pathways /." Access full-text from WCMC:, 2007. http://proquest.umi.com/pqdweb?did=1296119161&sid=8&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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25

Wright, Victoria M. "Investigating the differential properties of the Drosophila JAK/STAT pathway ligands." Thesis, University of Sheffield, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.555230.

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The JAK/STAT signalling cascade in vertebrates is activated in response to multiple cytokines and growth factors. By contrast, the Drosophila genome encodes for only three related JAK/STAT ligands, Upd, Upd2 and Upd3. It is hoped that identifying the differences in signalling stimulated by these three Updlike ligands will ultimately lead to a greater understanding of this disease-related pathway and its roles in development. Here, the analysis of the least well characterised of the Upd-like ligands, Upd3, is described. Upd3 is revealed as a secreted molecule that can activate JAK/STAT signalli
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26

Tang, Lingfeng. "THE JAK/STAT PATHWAY IS REUTILIZED IN DROSOPHILA SPERMATOGENESIS." UKnowledge, 2014. http://uknowledge.uky.edu/biology_etds/27.

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In the Drosophila testis, sperm are derived from germline stem cells (GSCs) which undergo a stereotyped pattern of divisions and differentiation. The somatic cells at the tip of the testis form the hub, which is the niche for both the somatic cyst stem cells (CySCs) and GSCs. The hub expresses Upd, a ligand for the JAK/STAT pathway that has roles in the maintenance of CySCs and GSCs. Male mutants of upd3, another ligand of the JAK/STAT pathway, become sterile much earlier than the wild-type, leading to the hypothesis that similar to upd, upd3 also promotes the self-renewal of stem cells in tes
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27

Lachance, Catherine. "LES INTERMÉDIAIRES DE LA VOIE JAK / STAT DANS LES SPERMATOZOÏDES HUMAINS." Thesis, Université Laval, 2013. http://www.theses.ulaval.ca/2013/29583/29583.pdf.

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28

Ning, Shunbin, and Ling Wang. "Inactivation Of Type I IFN Jak-STAT Pathway In EBV Latency." Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/etsu-works/6533.

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Epstein-Barr Virus (EBV) latent infection is associated with a variety of lymphomas and carcinomas. Interferon (IFN) Regulatory Factors (IRFs) are a family of transcription factors, among which IRF7 is the “master” regulator of type I IFNs (IFN-I) that defends against invading viruses. Robust IFN-I responses require a positive feedback loop between IRF7 and IFN-I. In recent years, we have discovered that IRF7 is significantly induced and activated by the principal EBV oncoprotein--Latent Membrane Protein 1 (LMP1); however, IRF7 fails to trigger robust IFN-I responses in EBV latency. We believe
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29

zhang, qifang. "Role of Jak/Stat pathway in the pathogenesis of breast cancer." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/41.

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The Jak/Stat signaling cascade mediates cell proliferation, differentiation, survival, apoptosis and immune responses. Aberrant activation of this pathway mediates neoplastic transformation and abnormal growth of many malignancies including breast cancer, the most common cancer among women, and the second leading cause of cancer deaths in women in United States. The mechanism by which the Jak/Stat pathway modulates the pathogenesis of breast cancer is unclear. This dissertation elucidates roles of Jak/Stat members that mediate the pathogenesis of breast cancer. For these studies, we used 4T1
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30

Saharinen, Pipsa. "Signaling through the Jak-Stat pathway : regulation of tyrosine kinase activity." Helsinki : University of Helsinki, 2002. http://ethesis.helsinki.fi/julkaisut/mat/bioti/vk/saharinen/.

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31

Iskounen, Thinhinane. "La voie JAK/STAT : cible potentielle pour une médecine personnalisée dans la sarcoïdose." Electronic Thesis or Diss., Paris 13, 2024. http://www.theses.fr/2024PA131020.

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La sarcoïdose est une granulomatose d'étiologie inconnue, caractérisée par la formation de granulomes immuns dans divers organes, principalement les poumons. La présentation clinique et l'évolution de la sarcoïdose sont variables. L'analyse génomique du sang périphérique des patients a montré que la voie de signalisation JAK/STAT est significativement représentée dans la sarcoïdose et est associée à la gravité de la maladie. Cependant, l'expression spatiale et temporelle des membres de la voie JAK/STAT dans le granulome est encore mal connue. Nous émettons l'hypothèse que l'activation de la vo
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32

Tardif, Nicolas. "Mechanosignaling through Caveolae : A New Role for the Control of JAK-STAT Signaling." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS337/document.

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Les cavéoles sont des invaginations en forme de coupelle à la membrane plasmique. Ces organelles multifonctionnelles jouent entre autres, un rôle clé dans la mécano-protection et la signalisation cellulaire. En effet, les cavéoles ont la faculté de s’aplanir en réponse à l’augmentation de la tension membranaire, afin de protéger la cellule des contraintes mécaniques. Les cavéoles jouant un rôle clé dans la signalisation cellulaire, nous avions émis l’hypothèse que le cycle mécano-dépendent de désassemblage/réassemblage des cavéoles constitue un interrupteur mécanique de certaines voies de sign
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33

Gandhi, Hetvi. "Early events in cytokine receptor signaling." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-135614.

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Ligand-activated signal transduction is a process critical to cell survival and function as it serves as a means of communication between the cells and their environment. Endocytosis is generally thought to down-regulate incoming signals by reducing the surface availability of receptors. However, increasing evidence in many systems suggests a notion which is referred to as the „signalling endosome" hypothesis - that endocytosis can also actively contribute to signalling apart from clearance of activated receptors and thereby attenuation of signalling. The functional aspect of signalling endoso
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34

Strickland, Janae. "The Role of STAT and the Jak/STAT Pathway In Mediating the Effects of Interleukin-6 on StAR Expression." Diss., CLICK HERE for online access, 2007. http://contentdm.lib.byu.edu/ETD/image/etd1781.pdf.

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35

Murtfeldt, Eric Robert. "Consequences of ectopic JAK/STAT pathway activation in the Drosophila male germline." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p1457319.

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Thesis (M.S.)--University of California, San Diego, 2008.<br>Title from first page of PDF file (viewed November 5, 2008). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 51).
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36

Lukashova, Viktoria. "Involvement of the Jak/STAT pathway in platelet-activating factor receptor signaling." Thèse, Sherbrooke : Université de Sherbrooke, 2003. http://savoirs.usherbrooke.ca/handle/11143/4173.

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37

Benham, Rebecca Sturtevant. "BDNF and JAK/STAT: partners in seizure-induced GABA-A receptor downregulation." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12281.

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Thesis (Ph.D.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.<br>Brain derived neurotrophic factor (BDNF) plays an important role in development, differentiation, and survival of neurons. However, alterations in BDNF expression also occur in a number of neurological disorder
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38

SILVA, Juan Luiz Coelho da. "Impacto clínico e laboratorial de mutações no gene ASXL1 em pacientes com neoplasias mieloproliferativas." Universidade Federal de Pernambuco, 2016. https://repositorio.ufpe.br/handle/123456789/19535.

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Submitted by Fabio Sobreira Campos da Costa (fabio.sobreira@ufpe.br) on 2017-07-12T15:39:14Z No. of bitstreams: 2 license_rdf: 811 bytes, checksum: e39d27027a6cc9cb039ad269a5db8e34 (MD5) Dissertação Juan Luiz Coelho da Silva.pdf: 2693101 bytes, checksum: b946d507d9f21698d6349e8ecf91e259 (MD5)<br>Made available in DSpace on 2017-07-12T15:39:14Z (GMT). No. of bitstreams: 2 license_rdf: 811 bytes, checksum: e39d27027a6cc9cb039ad269a5db8e34 (MD5) Dissertação Juan Luiz Coelho da Silva.pdf: 2693101 bytes, checksum: b946d507d9f21698d6349e8ecf91e259 (MD5) Previous issue date: 2016-03-11<br>FACEPE<br
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Talerico, Cassandra. "Temporal Activation of the JAK-STAT Pathway in Relation to Cardiac Gene Expression in a Mouse Model of Cardiac Dysfunction." Cleveland State University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=csu1197055735.

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40

Shen, Ying. "The JAK/STAT pathway in Drosophila hematopoiesis: function and regulatory mechanisms." Ohio : Ohio University, 2007. http://www.ohiolink.edu/etd/view.cgi?ohiou1194628059.

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41

Matlock, Jennifer Renee. "THE JAK-STAT PATHWAY IS REQUIRED FOR MULTIPLE EARLY EVENTS IN DROSOPHILA OOGENESIS." UKnowledge, 2002. http://uknowledge.uky.edu/gradschool_theses/205.

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The Janus kinase (JAK) pathway is an integral part of signaling through a variety of ligands and receptors in mammals. The extensive reutilization and pleiotropy of this pathway in vertebrate development is conserved in other animals as well. In Drosophila melanogaster, JAK signaling is involved in embryonic pattern formation, sex determination, larval blood cell development, wing venation, planar polarity in the eye, and formation of other adult structures. Here we describe several roles for JAK signaling in Drosophila oogenesis. The gene for a JAK pathway ligand, unpaired, is expressed speci
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42

Ruez, Richard. "Mécanotransduction par les cavéoles : rôle dans l'activation de stat3 par l'interferon alpha." Thesis, Paris 11, 2011. http://www.theses.fr/2011PA112232.

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Hypothèse : Notre équipe étudie le rôle, mal connu, du trafic membranaire dans le contrôle de l’activation de la voie de signalisation JAK/STAT par les interférons (IFN), une voie clé du contrôle des processus cancéreux. La liaison de l’IFN-a à son récepteur IFNAR active les kinases JAK1 et TYK2 puis des transducteurs de signal comme STAT1, antiprolifératif, ou STAT3, qui a un pouvoir oncogénique. Le laboratoire a démontré récemment que le trafic membranaire d’IFNAR détermine la spécificité du signal des différents IFNs.L’objet de cette thèse est l’étude du rôle des cavéoles dans ce contrôle.
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43

Rollin, Simon. "Modulation de la signalisation du récepteur du facteur d'activation plaquettaire par SOCS3." Thèse, Université de Sherbrooke, 2009. http://savoirs.usherbrooke.ca/handle/11143/4296.

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Le facteur d'activation plaquettaire (PAF) est un puissant médiateur pro-inflammatoire impliqué dans des processus physiologiques et pathologiques.Le PAF exerce ses effets suite à la liaison à son récepteur, le récepteur du PAF (PAFR), qui est un récepteur à sept domaines transmembranaires et couplé aux protéines G (RCPG). La signalisation du PAFR est en partie médiée par les protéines G et implique principalement des sous-unités G[indice inférieur [alpha]i] et G[indice inférieur [alpha]q] dans plusieurs types cellulaires.Le PAFR peut également activer des effecteurs variés : des canaux ioniq
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44

Secardin, Lise. "Modélisation des néoplasmes myéloprolifératifs grâce aux cellules souches induites à la pluripotence (IPSC)." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCC313/document.

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Les néoplasmes myéloprolifératifs (NMP) sont hémopathies malignes aboutissant à la surproduction d'une ou plusieurs lignées myéloïdes. Elles sont dues à l'acquisition de mutations sur l'axe de signalisation MPL/JAK2 incluant des mutations de JAK2V617F, de MPL et plus récemment de la calréticuline (CALR), dont les deux principales sont CALRdel52 et CALRins5. Ces mutations de signalisations peuvent être accompagnées de mutations de l'épigénétique, les plus importantes étant des mutations dans TET2. Le but de cette thèse était d'étudier le rôle des mutations de TET2 et de la calrdel52 dans les NM
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Paliouras, Grigorios Nikiforos. "Effect of ethanol on the Jak-Stat pathway : is this an NMDA mediated event?" Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=79062.

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Alcohol affects many neurochemical processes, causing long-lasting changes in both the adult and developing brain. The Jak-Stat transcriptional activation pathway plays a role in the control of neuronal proliferation, survival and differentiation, but the effects of ethanol on the system have not been fully elucidated. The goal of this project was to define the effects of acute and subchronic ethanol exposure on the expression of proteins in the Jak-Stat pathway, using cultured NG108-15 cells, and in addition, to test the hypothesis that these effects are mediated through the NMDA recep
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Yockell-Lelièvre, Julien. "Étude de la régulation transcriptionnelle de ICAM-1 : implication de la voie JAK/STAT." Thesis, Université Laval, 2010. http://www.theses.ulaval.ca/2010/27403/27403.pdf.

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Etter, Jonathan Parker. "Development of Inhibitors in the IL-6/GP130/JAK/STAT Pathway as Therapeutic Agents." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1376525461.

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Kördel, Kristin [Verfasser]. "Targeting JAK/STAT signalling for sensitization of colorectal cancer cells to chemoradiotherapy / Kristin Kördel." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2021. http://d-nb.info/123712896X/34.

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Gomes, Guilherme Wataru. "Expressão gênica dos transportadores de membrana ABCB1,ABCG2, SLC22A1 e SLCO1A2 em linhagens celulares tratadas com inibidor comercial da via JAK-STAT." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-16032016-095918/.

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INTRODUÇÃO: A desregulação da via de sinalização JAK-STAT é uma característica marcante das neoplasias mieloproliferativas (NMPs), doenças clonais da célula tronco hematopoética, dentre as quais encontra-se a mielofibrose (MF). Diversos inibidores de JAK foram desenvolvidos para o tratamento da MF e encontram-se em diferentes fases de desenvolvimento clínico. Devido ao seu desenvolvimento recente, pouco se sabe a respeito do papel de transportadores de membrana na farmacocinética desses compostos. Essas proteínas realizam o influxo e efluxo celular de substratos endógenos e xenobióticos, e alt
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Fagan, Erin A. "Identification of the presence and activity of the JAK-STAT pathway in canine solid tumors." Thesis, Virginia Tech, 2017. http://hdl.handle.net/10919/100859.

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Background: The JAK-STAT pathway is a cellular signaling pathway, which acts normally in humans and animals in the control of multiple important functions. Dysregulation of this pathway has been identified in human cancers, as well as a limited number of veterinary cancers. Objectives: The aims of this study were to identify the presence and tentative activity of components of the JAK-STAT pathway in selected canine tumors. Methods: Formalin-fixed, paraffin-embedded samples from mast cell tumors (MCT), hemangiosarcomas (HSA), thyroid carcinomas, and apocrine gland anal sac adenocarcinomas (AGA
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