Literatura científica selecionada sobre o tema "Inhibiteurs de JAK/STAT"
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Artigos de revistas sobre o assunto "Inhibiteurs de JAK/STAT"
El Jammal, Thomas, Mathieu Gerfaud-Valentin, Pascal Seve e Yvan Jamilloux. "Inhibiteurs de la signalisation JAK/STAT au cours des maladies rhumatologiques : un spectre grandissant". Revue du Rhumatisme 87, n.º 4 (julho de 2020): 261–72. http://dx.doi.org/10.1016/j.rhum.2020.01.032.
Texto completo da fonteSagez, F., M. Sawaf, J. Sibilia, H. Dumortier, F. Monneaux e 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 (novembro de 2016): A215. http://dx.doi.org/10.1016/s1169-8330(16)30522-1.
Texto completo da fonteColonne, Punsiri M., Marina E. Eremeeva e 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, n.º 9 (20 de junho de 2011): 3733–43. http://dx.doi.org/10.1128/iai.05008-11.
Texto completo da fonteBarry, Sean P. "JAK-STAT". JAK-STAT 1, n.º 2 (abril de 2012): 90–91. http://dx.doi.org/10.4161/jkst.20939.
Texto completo da fonteGalli Sanchez, Ana Paula, Tatiane Ester Aidar Fernandes e Gustavo Martelli Palomino. "The JAK-STAT Pathway and the JAK Inhibitors". Journal of Clinical Research in Dermatology 7, n.º 5 (30 de novembro de 2020): 1–6. http://dx.doi.org/10.15226/2378-1726/7/5/001128.
Texto completo da fonteMinaudo, Carla. "Vía JAK-STAT e inhibidores JAK". Dermatología Argentina 28, n.º 2 (1 de junho de 2022): 55–62. http://dx.doi.org/10.47196/da.v28i2.2324.
Texto completo da fonteLiu, Jia, Faping Wang e Fengming Luo. "The Role of JAK/STAT Pathway in Fibrotic Diseases: Molecular and Cellular Mechanisms". Biomolecules 13, n.º 1 (6 de janeiro de 2023): 119. http://dx.doi.org/10.3390/biom13010119.
Texto completo da fonteMirault, Tristan. "Risques cardiovasculaires des inhibiteurs de JAK". JMV-Journal de Médecine Vasculaire 47 (março de 2022): S40. http://dx.doi.org/10.1016/j.jdmv.2022.01.015.
Texto completo da fonteSchieler, Jarod M., e Jeffrey O. Henderson. "Treating a Dysregulated JAK/STAT Pathway in Cancer Cells". Journal of Student Research 5, n.º 1 (14 de abril de 2016): 11–17. http://dx.doi.org/10.47611/jsr.v5i1.282.
Texto completo da fonteZhan, Xinliang, Yan Wang e 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, n.º 4 (1 de abril de 2021): 605–11. http://dx.doi.org/10.1166/jbt.2021.2566.
Texto completo da fonteTeses / dissertações sobre o assunto "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.
Texto completo da fonteRefractory 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.
Texto completo da fonteThe 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.
Texto completo da fonteDawson, M. A. F. "JAK-STAT signalling at chromatin". Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598423.
Texto completo da fonteBroughton, 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.
Texto completo da fonteZhu, 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.
Texto completo da fonteVogt, Katja L. "Endocytic regulation of JAK/STAT signalling". Thesis, University of Sheffield, 2014. http://etheses.whiterose.ac.uk/6655/.
Texto completo da fonteMoore, Rachel. "Regulation of JAK/STAT signalling by endocytosis". Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/22459/.
Texto completo da fonteLeal, 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.
Texto completo da fonteRöder, Sabine. "Signaltransduktion durch JAK-STAT-Moleküle bei der Polyzythämia vera". [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972175741.
Texto completo da fonteLivros sobre o assunto "Inhibiteurs de JAK/STAT"
Nicholson, Sandra E., e Nicos A. Nicola, eds. JAK-STAT Signalling. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-242-1.
Texto completo da fonteAnastasis, Stephanou, ed. JAK-STAT pathway in disease. Austin, Tex: Landes Bioscience, 2009.
Encontre o texto completo da fonteDecker, Thomas, e Mathias Müller, eds. Jak-Stat Signaling : From Basics to Disease. Vienna: Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-0891-8.
Texto completo da fonteWilks, Andrew F., e 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.
Texto completo da fonteWilks, Andrew F. Intracellular signal transduction: The JAK-STAT pathway. New York: Springer, 1996.
Encontre o texto completo da fonteGoswami, Ritobrata. JAK-STAT Signaling in Diseases. Taylor & Francis Group, 2020.
Encontre o texto completo da fonteGoswami, Ritobrata. JAK-STAT Signaling in Diseases. CRC Press, 2020.
Encontre o texto completo da fonteStephanou, Anastasis, e Bell Richard H. Jr. JAK-STAT Pathway in Disease. Taylor & Francis Group, 2009.
Encontre o texto completo da fonteGoswami, Ritobrata. JAK-STAT Signaling in Diseases. Taylor & Francis Group, 2020.
Encontre o texto completo da fonteH, Bell Jr Richard. JAK-STAT Pathway in Disease. Taylor & Francis Group, 2009.
Encontre o texto completo da fonteCapítulos de livros sobre o assunto "Inhibiteurs de JAK/STAT"
Caldow, Marissa K., e 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.
Texto completo da fonteMeyer, Thomas, e 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.
Texto completo da fonteMeyer, Thomas, e 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.
Texto completo da fonteLeonard, 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.
Texto completo da fonteVangara, Bhavana S., e 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.
Texto completo da fonteStine, Rachel R., e 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.
Texto completo da fonteSiddiqui, M. A. Q., e 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.
Texto completo da fonteVogl, Claus, Priyank Shukla e 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.
Texto completo da fonteWilks, Andrew F., e 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.
Texto completo da fonteCroker, Ben A., e 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.
Texto completo da fonteTrabalhos de conferências sobre o assunto "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.
Texto completo da fonteFanouriakis, 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.
Texto completo da fonteElahi, Abul, Jonathan M. Hernandez e 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.
Texto completo da fonteMohbeddin, Abeer, Nawar Haj Ahmed e 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.
Texto completo da fonteDe 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.
Texto completo da fonteMontazeri Aliabadi, Hamidreza, Emira Bousoik e 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.
Texto completo da fonteClarke, DL, EL Hardaker, MC Catley, MA Birrell e 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.
Texto completo da fonteDenk, Dagmar, Klaus Fortschegger e 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.
Texto completo da fonteJingjing, Gong, Izhar S. Batth e 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.
Texto completo da fonteYew-Booth, Liang, Ming Sum Lau, Steven M. Evans, Iain Kilty, Maria G. Belvisi e 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.
Texto completo da fonteRelatórios de organizações sobre o assunto "Inhibiteurs de JAK/STAT"
Brooks-Kayal, Amy, e Bret Smith. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, julho de 2013. http://dx.doi.org/10.21236/ada612534.
Texto completo da fonteSmith, Bret N. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, setembro de 2014. http://dx.doi.org/10.21236/ada613987.
Texto completo da fonteBrooks-Kayal, Amy, Lauren Frey e Bret N. Smith. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, setembro de 2014. http://dx.doi.org/10.21236/ada614126.
Texto completo da fonteSmith, Bret N. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, julho de 2012. http://dx.doi.org/10.21236/ada568150.
Texto completo da fonteBrooks-Kayal, Amy. Jak/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, julho de 2012. http://dx.doi.org/10.21236/ada568663.
Texto completo da fonteSmith, Bret N. JaK/STAT Inhibition to Prevent Post-Traumatic Epileptogenesis. Fort Belvoir, VA: Defense Technical Information Center, julho de 2013. http://dx.doi.org/10.21236/ada586062.
Texto completo da fonteNeilson, Lynn. Prolactin Receptor Coupling to Jak-Stat Pathways in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, agosto de 2007. http://dx.doi.org/10.21236/ada485255.
Texto completo da fonteNeilson, Lynn. Prolactin Receptor Coupling to Jak-Stat Pathways in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, julho de 2007. http://dx.doi.org/10.21236/ada472476.
Texto completo da fonteClevenger, Charles V., e Anthony A. Kossiakoff. Use of Synthetic Antibodies Targeted to the Jak/Stat Pathway in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, março de 2011. http://dx.doi.org/10.21236/ada543162.
Texto completo da fonteClevenger, Charles. Use of Synthetic Antibodies Targeted to the Jak/Stat Pathway in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, março de 2010. http://dx.doi.org/10.21236/ada551381.
Texto completo da fonte