Relevant bibliographies by topics / Inhibiteurs de JAK/STAT

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Inhibiteurs de JAK/STAT'

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

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Journal articles on the topic "Inhibiteurs de JAK/STAT"

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El Jammal, Thomas, Mathieu Gerfaud-Valentin, Pascal Seve, and Yvan Jamilloux. "Inhibiteurs de la signalisation JAK/STAT au cours des maladies rhumatologiques : un spectre grandissant." Revue du Rhumatisme 87, no. 4 (2020): 261–72. http://dx.doi.org/10.1016/j.rhum.2020.01.032.

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Sagez, F., M. Sawaf, J. Sibilia, H. Dumortier, F. Monneaux, and J. E. Gottenberg. "Nouveau mécanisme d’action des inhibiteurs de la voie JAK/STAT : l’inhibition de la différenciation et de la fonction des lymphocytes T folliculaires auxiliaires." Revue du Rhumatisme 83 (November 2016): A215. http://dx.doi.org/10.1016/s1169-8330(16)30522-1.

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Colonne, Punsiri M., Marina E. Eremeeva, and Sanjeev K. Sahni. "Beta Interferon-Mediated Activation of Signal Transducer and Activator of Transcription Protein 1 Interferes with Rickettsia conorii Replication in Human Endothelial Cells." Infection and Immunity 79, no. 9 (2011): 3733–43. http://dx.doi.org/10.1128/iai.05008-11.

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ABSTRACTInfection of the endothelial cell lining of blood vessels withRickettsia conorii, the causative agent of Mediterranean spotted fever, results in endothelial activation. We investigated the effects ofR. conoriiinfection on the status of the Janus kinase (JAK)-signal transducer and activator of transcription protein (STAT) signaling pathway in human microvascular endothelial cells (HMECs), the most relevant host cell type, in light of rickettsial tropism for microvascular endotheliumin vivo.R. conoriiinfection induced phosphorylation of STAT1 on tyrosine 701 and serine 727 at 24, 48, and
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Barry, Sean P. "JAK-STAT." JAK-STAT 1, no. 2 (2012): 90–91. http://dx.doi.org/10.4161/jkst.20939.

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Galli Sanchez, Ana Paula, Tatiane Ester Aidar Fernandes, and Gustavo Martelli Palomino. "The JAK-STAT Pathway and the JAK Inhibitors." Journal of Clinical Research in Dermatology 7, no. 5 (2020): 1–6. http://dx.doi.org/10.15226/2378-1726/7/5/001128.

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Dozens of cytokines that bind Type I and Type II receptors use the Janus Kinases (JAK) and the Signal Transducer and Activator of Transcription (STAT) proteins pathway for intracellular signaling, orchestrating hematopoiesis, inducing inflammation, and controlling the immune response. Currently, oral JAK inhibitors are being used to treat many inflammatory and myeloproliferative diseases and are also under investigation in several clinical trials for skin diseases. Thus, dermatologists should understand how the JAK-STAT pathway works as well as the mechanism of action of the JAK inhibitors whi
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Liu, Jia, Faping Wang, and Fengming Luo. "The Role of JAK/STAT Pathway in Fibrotic Diseases: Molecular and Cellular Mechanisms." Biomolecules 13, no. 1 (2023): 119. http://dx.doi.org/10.3390/biom13010119.

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There are four members of the JAK family and seven of the STAT family in mammals. The JAK/STAT molecular pathway could be activated by broad hormones, cytokines, growth factors, and more. The JAK/STAT signaling pathway extensively mediates various biological processes such as cell proliferation, differentiation, migration, apoptosis, and immune regulation. JAK/STAT activation is closely related to growth and development, homeostasis, various solid tumors, inflammatory illness, and autoimmune diseases. Recently, with the deepening understanding of the JAK/STAT pathway, the relationship between
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Mirault, Tristan. "Risques cardiovasculaires des inhibiteurs de JAK." JMV-Journal de Médecine Vasculaire 47 (March 2022): S40. http://dx.doi.org/10.1016/j.jdmv.2022.01.015.

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Minaudo, Carla. "Vía JAK-STAT e inhibidores JAK." Dermatología Argentina 28, no. 2 (2022): 55–62. http://dx.doi.org/10.47196/da.v28i2.2324.

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La vía JAK-STAT (Janus Kinasas) es una cadena de traducción de señales intracelulares, que se activa a través de receptores de citoquinas I y II. Mediante esta vía, varias moléculas de importancia en dermatología ejercen sus efectos: IL2, IL4, IL7, IL5, IL6, IL9, IL12, IL13, IL15, IL21, IL23, INFa e INFb, entre otras. También es la señal intracelular de hormonas como la prolactina y la hormona de crecimiento. La inhibición de distintos componentes de esta vía es utilizada como terapéutica en enfermedades reumatológicas y un número cada vez mayor de patologías cutáneas. Los inhibidores JAK surg
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Schieler, Jarod M., and Jeffrey O. Henderson. "Treating a Dysregulated JAK/STAT Pathway in Cancer Cells." Journal of Student Research 5, no. 1 (2016): 11–17. http://dx.doi.org/10.47611/jsr.v5i1.282.

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The JAK/STAT pathway is induced by the binding of a cytokine to its cognate receptor. The receptor’s engagement with the cytokine recruits a JAK protein, which activates itself via auto/trans-phosphorylation. In turn, the activated JAKs recruit and phosphorylate STAT proteins. The phosphorylated STAT proteins form a dimer, translocate to the cell nucleus and acts as a transcription factor to induce gene expression. In this way, the JAK/STAT pathway can mediate a cell’s response to extracellular signals. The proteins ultimately induced by the JAK/STAT pathway contribute to processes such as inf
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Zhan, Xinliang, Yan Wang, and Jing Yang. "Janus Kinase/Signal Converters, and the Transcriptional Activator Signaling Pathway Promotes Lung Cancer Through Increasing M2 Macrophage." Journal of Biomaterials and Tissue Engineering 11, no. 4 (2021): 605–11. http://dx.doi.org/10.1166/jbt.2021.2566.

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Accumulating evidence highlights the salient function of JAK/STAT signaling pathway in tumorigenesis and development. But the mechanism of JAK/STAT signaling in lung cancer remains elusive. This study assessed the impact of JAK/STAT on lung tumorigenesis and its interaction with microenvironment. Mouse model of primary lung cancer was established and then treated with JAK/STAT inhibitor. Immunofluorescence was performed to analyze fluorescent labels. Transwell assay determined the cell migration ability, and Western blot, immunohistochemistry, and immunofluorescence to detect the expression of
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Dissertations / Theses on the topic "Inhibiteurs de JAK/STAT"

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

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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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Books on the topic "Inhibiteurs de JAK/STAT"

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Nicholson, Sandra E., and Nicos A. Nicola, eds. JAK-STAT Signalling. Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-242-1.

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Anastasis, Stephanou, ed. JAK-STAT pathway in disease. Landes Bioscience, 2009.

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Decker, Thomas, and Mathias Müller, eds. Jak-Stat Signaling : From Basics to Disease. Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-0891-8.

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Wilks, Andrew F., and Ailsa G. Harpur. Intracellular Signal Transduction: The JAK-STAT Pathway. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22050-4.

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Wilks, Andrew F. Intracellular signal transduction: The JAK-STAT pathway. Springer, 1996.

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Köberlein, Bernd. Interaktion von Hepatitis-B- und -C-Viren mit der inflammatorischen JAK-STAT-Signaltransduktion. B. Köberlein, 2008.

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Goswami, Ritobrata. JAK-STAT Signaling in Diseases. Taylor & Francis Group, 2020.

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Goswami, Ritobrata. JAK-STAT Signaling in Diseases. CRC Press, 2020.

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Stephanou, Anastasis, and Bell Richard H. Jr. JAK-STAT Pathway in Disease. Taylor & Francis Group, 2009.

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Goswami, Ritobrata. JAK-STAT Signaling in Diseases. Taylor & Francis Group, 2020.

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Book chapters on the topic "Inhibiteurs de JAK/STAT"

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Caldow, Marissa K., and David Cameron-Smith. "JAK/STAT Pathway." In Encyclopedia of Exercise Medicine in Health and Disease. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_242.

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Meyer, Thomas, and Uwe Vinkemeier. "JAK-STAT Pathway." In Encyclopedia of Molecular Pharmacology. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-21573-6_157-1.

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Meyer, Thomas, and Uwe Vinkemeier. "JAK-STAT Pathway." In Encyclopedia of Molecular Pharmacology. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57401-7_157.

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Leonard, Warren J. "The JAK-STAT Pathway." In Hormone Signaling. Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-3600-7_6.

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Vangara, Bhavana S., and Jennifer R. Grandis. "Jak/STAT Signaling in HNC." In Molecular Determinants of Head and Neck Cancer. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8815-6_8.

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Larner, Andrew C., and Andrew Keightley. "The Jak/Stat Signaling Cascade." In Signaling Networks and Cell Cycle Control. Humana Press, 2000. https://doi.org/10.1007/978-1-59259-218-0_21.

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Stine, Rachel R., and Erika L. Matunis. "JAK-STAT Signaling in Stem Cells." In Transcriptional and Translational Regulation of Stem Cells. Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6621-1_14.

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Siddiqui, M. A. Q., and Eduardo Mascareno. "JAK/Stat Signaling in Cardiac Diseases." In Signal Transduction and Cardiac Hypertrophy. Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0347-7_25.

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Vogl, Claus, Priyank Shukla, and Ingo Ebersberger. "Evolution of Jak and Stat Proteins." In Jak-Stat Signaling : From Basics to Disease. Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-0891-8_7.

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Büyükafşar, Kansu. "History of JAK/STAT Pathway at a Glance." In Jak-Inhibitors in Dermatology. Springer Nature Switzerland, 2025. https://doi.org/10.1007/978-3-031-84274-0_1.

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Conference papers on the topic "Inhibiteurs de JAK/STAT"

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Beeckmans, H., J. E. Mcdonough, L. De Sadeleer, et al. "JAK-STAT pathway is upregulated in CLAD." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.1390.

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Fanouriakis, Antonis. "28 JAK-STAT inhibitors in systemic lupus erythematosus." In 12th Annual Meeting of the Lupus Academy; Virtual Pre-meeting: September 1, 2023; Hybrid Annual Meeting (Barcelona): September 8–10, 2023. Lupus Foundation of America, 2023. http://dx.doi.org/10.1136/lupus-2023-la.28.

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Elahi, Abul, Jonathan M. Hernandez, and David Shibata. "Abstract 3064: HPP1 tumor suppression and JAK-STAT signaling." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3064.

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Bing, TJ, Peng Liu, and Lili Chai. "850 JAK-STAT platform for immune-related drug discovery." In SITC 39th Annual Meeting (SITC 2024) Abstracts. BMJ Publishing Group Ltd, 2024. http://dx.doi.org/10.1136/jitc-2024-sitc2024.0850.

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Mohbeddin, Abeer, Nawar Haj Ahmed, and Layla Kamareddine. "The use of Drosophila Melanogaster as a Model Organism to study the effect of Innate Immunity on Metabolism." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0224.

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Apart from its traditional role in disease control, recent body of evidence has implicated a role of the immune system in regulating metabolic homeostasis. Owing to the importance of this “immune-metabolic alignment” in dictating a state of health or disease, a proper mechanistic understanding of this alignment is crucial in opening up for promising therapeutic approaches against a broad range of chronic, metabolic, and inflammatory disorders like obesity, diabetes, and inflammatory bowel syndrome. In this project, we addressed the role of the Janus kinase/signal transducer and activator of tr
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Nayak, Barsha Baisakhi, Julia Teppan, Iris Red, Juliana Schwanzer, Akos Heinemann, and Eva Böhm. "The role of JAK/STAT signaling in neutrophilic airway inflammation." In ERS Congress 2024 abstracts. European Respiratory Society, 2024. http://dx.doi.org/10.1183/13993003.congress-2024.pa4858.

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De Velasco, Marco A., Yurie Kura, Naomi Ando, et al. "Abstract 906: Therapeutic potential of JAK/STAT signal inhibition in prostate cancer by the JAK inhibitor AZD1480." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-906.

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Montazeri Aliabadi, Hamidreza, Emira Bousoik, and Parvin Mahdipoor. "Abstract B087: A systematic approach to JAK/STAT pathway shut-down." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-b087.

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Clarke, DL, EL Hardaker, MC Catley, MA Birrell, and MG Belvisi. "Inhibition of JAK/STAT Signalling: A Novel Therapy for Steroid Resistant Asthma?." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5599.

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Denk, Dagmar, Klaus Fortschegger, and Sabine Strehl. "Abstract 2171: The fusion protein PAX5-JAK2 constitutively activates JAK-STAT signaling." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2171.

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Reports on the topic "Inhibiteurs de JAK/STAT"

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Brooks-Kayal, Amy, and Bret Smith. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada612534.

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Smith, Bret N. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Defense Technical Information Center, 2014. http://dx.doi.org/10.21236/ada613987.

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Brooks-Kayal, Amy, Lauren Frey, and Bret N. Smith. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Defense Technical Information Center, 2014. http://dx.doi.org/10.21236/ada614126.

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Smith, Bret N. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada568150.

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Brooks-Kayal, Amy. Jak/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada568663.

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Smith, Bret N. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada586062.

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Neilson, Lynn. Prolactin Receptor Coupling to Jak-Stat Pathways in Breast Cancer. Defense Technical Information Center, 2007. http://dx.doi.org/10.21236/ada485255.

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Neilson, Lynn. Prolactin Receptor Coupling to Jak-Stat Pathways in Breast Cancer. Defense Technical Information Center, 2007. http://dx.doi.org/10.21236/ada472476.

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Clevenger, Charles V., and Anthony A. Kossiakoff. Use of Synthetic Antibodies Targeted to the Jak/Stat Pathway in Breast Cancer. Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada543162.

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Clevenger, Charles. Use of Synthetic Antibodies Targeted to the Jak/Stat Pathway in Breast Cancer. Defense Technical Information Center, 2010. http://dx.doi.org/10.21236/ada551381.

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