Auswahl der wissenschaftlichen Literatur zum Thema „Inhibiteurs de JAK/STAT“
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Zeitschriftenartikel zum Thema "Inhibiteurs de JAK/STAT"
El Jammal, Thomas, Mathieu Gerfaud-Valentin, Pascal Seve und Yvan Jamilloux. „Inhibiteurs de la signalisation JAK/STAT au cours des maladies rhumatologiques : un spectre grandissant“. Revue du Rhumatisme 87, Nr. 4 (Juli 2020): 261–72. http://dx.doi.org/10.1016/j.rhum.2020.01.032.
Der volle Inhalt der QuelleSagez, F., M. Sawaf, J. Sibilia, H. Dumortier, F. Monneaux und 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.
Der volle Inhalt der QuelleColonne, Punsiri M., Marina E. Eremeeva und 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, Nr. 9 (20.06.2011): 3733–43. http://dx.doi.org/10.1128/iai.05008-11.
Der volle Inhalt der QuelleBarry, Sean P. „JAK-STAT“. JAK-STAT 1, Nr. 2 (April 2012): 90–91. http://dx.doi.org/10.4161/jkst.20939.
Der volle Inhalt der QuelleGalli Sanchez, Ana Paula, Tatiane Ester Aidar Fernandes und Gustavo Martelli Palomino. „The JAK-STAT Pathway and the JAK Inhibitors“. Journal of Clinical Research in Dermatology 7, Nr. 5 (30.11.2020): 1–6. http://dx.doi.org/10.15226/2378-1726/7/5/001128.
Der volle Inhalt der QuelleMinaudo, Carla. „Vía JAK-STAT e inhibidores JAK“. Dermatología Argentina 28, Nr. 2 (01.06.2022): 55–62. http://dx.doi.org/10.47196/da.v28i2.2324.
Der volle Inhalt der QuelleLiu, Jia, Faping Wang und Fengming Luo. „The Role of JAK/STAT Pathway in Fibrotic Diseases: Molecular and Cellular Mechanisms“. Biomolecules 13, Nr. 1 (06.01.2023): 119. http://dx.doi.org/10.3390/biom13010119.
Der volle Inhalt der QuelleMirault, Tristan. „Risques cardiovasculaires des inhibiteurs de JAK“. JMV-Journal de Médecine Vasculaire 47 (März 2022): S40. http://dx.doi.org/10.1016/j.jdmv.2022.01.015.
Der volle Inhalt der QuelleSchieler, Jarod M., und Jeffrey O. Henderson. „Treating a Dysregulated JAK/STAT Pathway in Cancer Cells“. Journal of Student Research 5, Nr. 1 (14.04.2016): 11–17. http://dx.doi.org/10.47611/jsr.v5i1.282.
Der volle Inhalt der QuelleZhan, Xinliang, Yan Wang und 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, Nr. 4 (01.04.2021): 605–11. http://dx.doi.org/10.1166/jbt.2021.2566.
Der volle Inhalt der QuelleDissertationen zum Thema "Inhibiteurs de JAK/STAT"
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.
Der volle Inhalt der QuelleRefractory coeliac disease type II (RCDII), also called intraepithelial lymphoma, is a rare but severe complication of coeliac disease characterized by the clonal expansion of a small subset of innate intraepithelial lymphocytes (IEL), present in the normal human and murine intestine. Our lab has shown that this population displays shared features between T and natural killer (NK) cells. These so-called iCD3+ innate IEL are mainly characterized by intracellular expression of CD3, which is not detected at the cell surface, expression of NK receptors as well as DNA rearrangement of T cell receptor genes. Our lab has also shown that iCD3+ innate IEL originate from bone marrow precursors through coordinated NOTCH1 and interleukin (IL)-15 signals. During lymphomagenesis, iCD3+ innate IEL of most RCDII patients were shown to have acquired somatic gain-of-function mutations in JAK1 and/or STAT3 that confer increased sensitivity to interleukin-15, a cytokine overexpressed in the intestine of coeliac patients, thereby promoting their clonal expansion. Thus, our hypothesis is that JAK1/STAT3 mutations play a key role in initiating lymphomagenesis associated to coeliac disease in an IL-15-rich environment and that they could represent an attractive therapeutic target.The first objective of my thesis was to study the interest of JAK/STAT inhibitors for RCDII treatment. First, we have tested in vitro different JAK/STAT inhibitors on IL-15-dependent RCDII or normal IEL-T cell lines. We have shown that these inhibitors decrease the proliferation and phosphorylation of STAT3 and increase cellular apoptosis in both RCDII and normal T cell lines. Secondly, we have established a xenograft model based on the injection of cells derived from biopsy or blood from one RCDII patient into immunodeficient mice overexpressing the human IL-15 transgene in their gut epithelium (Rag-/-Gc-/- IL-15TgE; IRGC) to test the efficacy of JAK/STAT inhibitors in vivo. Treatment of xenografted mice with ruxolitinib, a potent inhibitor of JAK1/JAK2 decreased the frequency, number and cytotoxic potential of human tumoral cells and allowed clinical restoration. These preliminary results are encouraging but need to be confirmed. The second objective of my thesis was to test whether the Stat3 pD661V mutation is sufficient to induce the intraepithelial lymphoma in an IL-15-rich context in IRGC mice. We have successfully generated murine iCD3+ innate IEL in vitro, resembling their human counterparts from common lymphoid precursors by combining NOTCH and IL-15 signals. We then transduced CLP with a retroviral vector containing wild-type or mutated Stat3 pD661V. The transduced cells were injected into IRGC mice that subsequently were followed-up during a period of 8 weeks. In vitro generated iCD3+ innate IEL preferentially homed to the intestine. However, no development of intraepithelial lymphoma was observed suggesting that the Stat3 pD661V variant alone is not sufficient to induce the intraepithelial lymphoma. These preliminary results need to be reproduced and confirmed. The murine model used to test the role of STAT3 will now be used to evaluate the respective contribution of canonical mutations in JAK1 and STAT3 and of other recurrent mutations identified in RCDII
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.
Der volle Inhalt der QuelleThe LNK adaptor protein is a key negative regulator of signalling pathways, such as JAK/STAT, important in the development of the hematopoietic system. Its implication in chronic blood diseases, such as Myeloproliferative Neoplasms (MPN) has been confirmed by studies on Lnk-deficient mice, as well as the identification of LNK mutations in MPN patients. However, the LNK mechanism of regulation on its partners and the functional implication of LNK mutations in MPN pathogenesis, are still unclear. Therefore, my PhD project covers the structural and functional analysis of theLNK/JAK2 signalling complex and the development of a molecular strategy to use LNK as a therapeutic tool for the treatment of MPN patients. Our study showed, for the first time, the inhibitory function of the N-terminal region and the pleckstrin homology domain of LNK on JAK2 activity, which occurs more importantly on JAK-V617F than JAK2 wild type form. Moreover, our study provided evidence on how LNK mutations located in this LNK region could contribute to these haematological diseases and has allowed us to propose a model for LNK regulatory function on JAK2activity. Furthermore, we developed a cell penetrating peptide-based strategy to deliver this regulatory region of LNK in hematopoietic cells to specifically inhibit JAK2-V617F oncogenic form. The finalaim is to use this region as a therapeutic molecule to treat JAK2-V617F-positive MPN patients
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.
Der volle Inhalt der QuelleDawson, M. A. F. „JAK-STAT signalling at chromatin“. Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598423.
Der volle Inhalt der QuelleBroughton, 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.
Der volle Inhalt der QuelleZhu, 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.
Der volle Inhalt der QuelleVogt, Katja L. „Endocytic regulation of JAK/STAT signalling“. Thesis, University of Sheffield, 2014. http://etheses.whiterose.ac.uk/6655/.
Der volle Inhalt der QuelleMoore, Rachel. „Regulation of JAK/STAT signalling by endocytosis“. Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/22459/.
Der volle Inhalt der QuelleLeal, 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.
Der volle Inhalt der QuelleRöder, Sabine. „Signaltransduktion durch JAK-STAT-Moleküle bei der Polyzythämia vera“. [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972175741.
Der volle Inhalt der QuelleBücher zum Thema "Inhibiteurs de JAK/STAT"
Nicholson, Sandra E., und Nicos A. Nicola, Hrsg. JAK-STAT Signalling. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-242-1.
Der volle Inhalt der QuelleAnastasis, Stephanou, Hrsg. JAK-STAT pathway in disease. Austin, Tex: Landes Bioscience, 2009.
Den vollen Inhalt der Quelle findenDecker, Thomas, und Mathias Müller, Hrsg. Jak-Stat Signaling : From Basics to Disease. Vienna: Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-0891-8.
Der volle Inhalt der QuelleWilks, Andrew F., und Ailsa G. Harpur. Intracellular Signal Transduction: The JAK-STAT Pathway. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22050-4.
Der volle Inhalt der QuelleWilks, Andrew F. Intracellular signal transduction: The JAK-STAT pathway. New York: Springer, 1996.
Den vollen Inhalt der Quelle findenGoswami, Ritobrata. JAK-STAT Signaling in Diseases. Taylor & Francis Group, 2020.
Den vollen Inhalt der Quelle findenGoswami, Ritobrata. JAK-STAT Signaling in Diseases. CRC Press, 2020.
Den vollen Inhalt der Quelle findenStephanou, Anastasis, und Bell Richard H. Jr. JAK-STAT Pathway in Disease. Taylor & Francis Group, 2009.
Den vollen Inhalt der Quelle findenGoswami, Ritobrata. JAK-STAT Signaling in Diseases. Taylor & Francis Group, 2020.
Den vollen Inhalt der Quelle findenH, Bell Jr Richard. JAK-STAT Pathway in Disease. Taylor & Francis Group, 2009.
Den vollen Inhalt der Quelle findenBuchteile zum Thema "Inhibiteurs de JAK/STAT"
Caldow, Marissa K., und David Cameron-Smith. „JAK/STAT Pathway“. In Encyclopedia of Exercise Medicine in Health and Disease, 495–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_242.
Der volle Inhalt der QuelleMeyer, Thomas, und Uwe Vinkemeier. „JAK-STAT Pathway“. In Encyclopedia of Molecular Pharmacology, 1–5. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-21573-6_157-1.
Der volle Inhalt der QuelleMeyer, Thomas, und Uwe Vinkemeier. „JAK-STAT Pathway“. In Encyclopedia of Molecular Pharmacology, 889–93. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57401-7_157.
Der volle Inhalt der QuelleLeonard, Warren J. „The JAK-STAT Pathway“. In Hormone Signaling, 103–20. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-3600-7_6.
Der volle Inhalt der QuelleVangara, Bhavana S., und Jennifer R. Grandis. „Jak/STAT Signaling in HNC“. In Molecular Determinants of Head and Neck Cancer, 163–77. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8815-6_8.
Der volle Inhalt der QuelleStine, Rachel R., und Erika L. Matunis. „JAK-STAT Signaling in Stem Cells“. In Transcriptional and Translational Regulation of Stem Cells, 247–67. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6621-1_14.
Der volle Inhalt der QuelleSiddiqui, M. A. Q., und Eduardo Mascareno. „JAK/Stat Signaling in Cardiac Diseases“. In Signal Transduction and Cardiac Hypertrophy, 349–56. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0347-7_25.
Der volle Inhalt der QuelleVogl, Claus, Priyank Shukla und Ingo Ebersberger. „Evolution of Jak and Stat Proteins“. In Jak-Stat Signaling : From Basics to Disease, 99–114. Vienna: Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-0891-8_7.
Der volle Inhalt der QuelleWilks, Andrew F., und Ailsa G. Harpur. „STFs: STAT-Containing Transcription Factors“. In Intracellular Signal Transduction: The JAK-STAT Pathway, 79–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22050-4_5.
Der volle Inhalt der QuelleCroker, Ben A., und Nicos A. Nicola. „The Jak-Stat Pathway of Cytokine Signaling“. In Hematopoietic Growth Factors in Oncology, 45–64. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-747-5_3.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "Inhibiteurs de JAK/STAT"
Beeckmans, H., J. E. Mcdonough, L. De Sadeleer, A. Sacreas, A. Vanstapel, J. Kaes, A. Van Herck 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.
Der volle Inhalt der QuelleFanouriakis, 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.
Der volle Inhalt der QuelleElahi, Abul, Jonathan M. Hernandez und 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.
Der volle Inhalt der QuelleMohbeddin, Abeer, Nawar Haj Ahmed und 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.
Der volle Inhalt der QuelleDe Velasco, Marco A., Yurie Kura, Naomi Ando, Emiko Fukushima, Yuji Hatanaka, Yutaka Yamamoto, Nobutaka Shimizu 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.
Der volle Inhalt der QuelleMontazeri Aliabadi, Hamidreza, Emira Bousoik und 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.
Der volle Inhalt der QuelleClarke, DL, EL Hardaker, MC Catley, MA Birrell und 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.
Der volle Inhalt der QuelleDenk, Dagmar, Klaus Fortschegger und 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.
Der volle Inhalt der QuelleJingjing, Gong, Izhar S. Batth und Addanki P. Kumar. „Abstract 3544: Jak/Stat signaling: A potential target for pancreatic cancer management“. 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.am2011-3544.
Der volle Inhalt der QuelleYew-Booth, Liang, Ming Sum Lau, Steven M. Evans, Iain Kilty, Maria G. Belvisi und Mark A. Birrell. „Activation Of The JAK/STAT Pathway In The Lungs Of COPD Patients“. In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4546.
Der volle Inhalt der QuelleBerichte der Organisationen zum Thema "Inhibiteurs de JAK/STAT"
Brooks-Kayal, Amy, und Bret Smith. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, Juli 2013. http://dx.doi.org/10.21236/ada612534.
Der volle Inhalt der QuelleSmith, Bret N. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada613987.
Der volle Inhalt der QuelleBrooks-Kayal, Amy, Lauren Frey und Bret N. Smith. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada614126.
Der volle Inhalt der QuelleSmith, Bret N. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, Juli 2012. http://dx.doi.org/10.21236/ada568150.
Der volle Inhalt der QuelleBrooks-Kayal, Amy. Jak/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, Juli 2012. http://dx.doi.org/10.21236/ada568663.
Der volle Inhalt der QuelleSmith, Bret N. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, Juli 2013. http://dx.doi.org/10.21236/ada586062.
Der volle Inhalt der QuelleNeilson, Lynn. Prolactin Receptor Coupling to Jak-Stat Pathways in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2007. http://dx.doi.org/10.21236/ada485255.
Der volle Inhalt der QuelleNeilson, Lynn. Prolactin Receptor Coupling to Jak-Stat Pathways in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, Juli 2007. http://dx.doi.org/10.21236/ada472476.
Der volle Inhalt der QuelleClevenger, Charles V., und Anthony A. Kossiakoff. Use of Synthetic Antibodies Targeted to the Jak/Stat Pathway in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, März 2011. http://dx.doi.org/10.21236/ada543162.
Der volle Inhalt der QuelleClevenger, Charles. Use of Synthetic Antibodies Targeted to the Jak/Stat Pathway in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, März 2010. http://dx.doi.org/10.21236/ada551381.
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