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Artykuły w czasopismach na temat "Granzymes"
Joeckel, Lars T., i Phillip I. Bird. "Are all granzymes cytotoxic in vivo?" Biological Chemistry 395, nr 2 (1.02.2014): 181–202. http://dx.doi.org/10.1515/hsz-2013-0238.
Pełny tekst źródłaEbnet, K., C. N. Levelt, T. T. Tran, K. Eichmann i M. M. Simon. "Transcription of granzyme A and B genes is differentially regulated during lymphoid ontogeny." Journal of Experimental Medicine 181, nr 2 (1.02.1995): 755–63. http://dx.doi.org/10.1084/jem.181.2.755.
Pełny tekst źródłaHay, Zachary L. Z., i Jill E. Slansky. "Granzymes: The Molecular Executors of Immune-Mediated Cytotoxicity". International Journal of Molecular Sciences 23, nr 3 (6.02.2022): 1833. http://dx.doi.org/10.3390/ijms23031833.
Pełny tekst źródłaGrossman, William J., James W. Verbsky, Benjamin L. Tollefsen, Claudia Kemper, John P. Atkinson i Timothy J. Ley. "Differential expression of granzymes A and B in human cytotoxic lymphocyte subsets and T regulatory cells". Blood 104, nr 9 (1.11.2004): 2840–48. http://dx.doi.org/10.1182/blood-2004-03-0859.
Pełny tekst źródłaZeberg, Lennart, i Tor Olofsson. "Differential Expression of Granzymes A and K in Subsets of Human T-Cells and NK-Cells." Blood 106, nr 11 (16.11.2005): 3917. http://dx.doi.org/10.1182/blood.v106.11.3917.3917.
Pełny tekst źródłaCao, Xuefang, Paula A. Revell, William J. Grossman, Dori A. Thomas, Zhi Hong Lu i Timothy J. Ley. "Orphan Granzymes Downstream from Granzyme B Are Important for Tumor Clearance In Vivo and in Vitro." Blood 104, nr 11 (16.11.2004): 2653. http://dx.doi.org/10.1182/blood.v104.11.2653.2653.
Pełny tekst źródłaKaiserman, Dion, Catherina H. Bird, Jiuru Sun, Antony Matthews, Kheng Ung, James C. Whisstock, Philip E. Thompson, Joseph A. Trapani i Phillip I. Bird. "The major human and mouse granzymes are structurally and functionally divergent". Journal of Cell Biology 175, nr 4 (20.11.2006): 619–30. http://dx.doi.org/10.1083/jcb.200606073.
Pełny tekst źródłaThiery, Jerome, Dennis Keefe, Saviz Saffarian, Denis Martinvalet, Michael Walch, Emmanuel Boucrot, Tomas Kirchhausen i Judy Lieberman. "Perforin activates clathrin- and dynamin-dependent endocytosis, which is required for plasma membrane repair and delivery of granzyme B for granzyme-mediated apoptosis". Blood 115, nr 8 (25.02.2010): 1582–93. http://dx.doi.org/10.1182/blood-2009-10-246116.
Pełny tekst źródłaNakajima, H., H. L. Park i P. A. Henkart. "Synergistic roles of granzymes A and B in mediating target cell death by rat basophilic leukemia mast cell tumors also expressing cytolysin/perforin." Journal of Experimental Medicine 181, nr 3 (1.03.1995): 1037–46. http://dx.doi.org/10.1084/jem.181.3.1037.
Pełny tekst źródłaGriffiths, G. M., i S. Isaaz. "Granzymes A and B are targeted to the lytic granules of lymphocytes by the mannose-6-phosphate receptor." Journal of Cell Biology 120, nr 4 (15.02.1993): 885–96. http://dx.doi.org/10.1083/jcb.120.4.885.
Pełny tekst źródłaRozprawy doktorskie na temat "Granzymes"
Yang, Jie. "Characterization of bovine granzymes and studies of the role of granzyme B in killing of Theileria-infected cells by CD8+ T cells". Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6487.
Pełny tekst źródłaTinangon, Maria M. "Strategies to identify granzyme J /". abstract and full text PDF (UNR users only), 2001. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:1404986.
Pełny tekst źródłaKoot, Gretchen E. "Serine and cysteine protease inhibitors for blockade of cell mediated cytotoxicity /". abstract and full text PDF (UNR users only), 2002. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3121138.
Pełny tekst źródłaBen, Safta Thouraya. "Implication de la protéine suppresseur de tumeurs p53 dans la mort cellulaire induite par les lymphocytes T cytotoxiques et les cellules NK : rôle dans la régulation de l’apoptose dépendante du granzyme B". Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS162/document.
Pełny tekst źródłaCytotoxic T lymphocytes (CTL) and natural killer (NK) cells eliminate their tumor target cells through exocytosis and release of the cytotoxic granules (CG) content. These CG contain a pore-forming protein called perforin (PFN), and a family of cell death inducing serine-proteases, called granzymes (Gzms). Gzms enter the target cells in a PFN-dependent manner and activate various apoptotic signaling pathways leading to the death of the target cell. In this work, we studied the role of the tumor suppressor protein p53 in the molecular cascade leading to apoptosis induced by cytotoxic effectors via the PFN/Granzyme B (GzmB) pathway. We have shown that in response to GzmB or to cytotoxic effectors, wild-type p53 accumulates on target mitochondria in order to interact with the anti-apoptotic protein Bcl-2 and to positively regulate the GzmB-induced mitochondrial outer membrane permeabilization. Thus, the non-transcriptional activity of p53 in the mitochondria plays a key role in the control of apoptosis induced by CTL and NK (Ben Safta et al J Immunol 2015). Because the TP53 gene is mutated in more than 50% of human tumors, we also aimed to determine whether the restoration of a wild-type p53 fonction in tumor cells carrying a non-functional p53 could potentiate the cytotoxic antitumor response. Our results show that the pharmacological reactivation of a wild-type p53 activity in a mammary adenocarcinoma cell line harboring a mutated p53 sensitize these tumor cells to the NK cell lysis via the activation of autophagy and a cascade of molecular events that are being identified
LAFAURIE, CLOTILDE. "Etude de la regulation de la transcription et de l'expression des genes des granzymes b et h humains". Paris 11, 1997. http://www.theses.fr/1997PA112327.
Pełny tekst źródłaMouchacca, Pierre. "Granzyme B-td TOMATO, un nouvel outil fluorescent pour le suivi de la cytolyse chez la souris". Thesis, Aix-Marseille, 2012. http://www.theses.fr/2012AIXM4008/document.
Pełny tekst źródłaCytolysis is a major function used by the immune system's effectors to kill infected or tumor cells. Cytolysis depends on the pore forming protein perforin and the secretion of proteases of the granzyme family. Granzymes, including granzyme B (GZMB) have pro-apoptotic features and induce target cell death. Several complementary pathways are triggered by granzymes to ensure efficient cytolysis. It remains difficult to directly observe cytolysis during in vivo immune responses under physiological conditions. In this PhD we developed a new model to visualize cytolytic function in real time by expression of a fusion protein: GZMB-tdTomato. Results obtained from retroviral transduction showed that the fusion protein is correctly expressed in cytolytic vesicles, which became fluorescent. We then constructed a new mouse model by homologous recombination (Knock In) that express GZMB-tdTomato substituted for the native GZMB. The fusion protein conserves the catalytic activity of GZMB and its features (expression, maturation, secretion conditions) and remains active after its passage into target cells. Using TCR transgenic OTI cells, we followed the sequence of events of cytolysis from lymphocytes in real time by videomicroscopy. We also observed the cytolytic vesicles relocalization towards the cell contact zone and the death of target cell by cytolysis. Finally, we studied in vivo differentiation of naïve lymphocyte to cytolytic effector cells (the acquisition of cytolysis) and target cell death after bacterial infection
Sumaria, Nital. "The relevance of specific molecular and cellular effectors during murine cytomegalovirus infection". University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0116.
Pełny tekst źródłaBenechet, Alexandre. "Dynamic of the effector T cells egress from secondary lymphoid organs after infection". Paris 7, 2014. http://www.theses.fr/2014PA077126.
Pełny tekst źródłaAn effective immune response depends on the large-scale, but carefully regulated migration of cells within and between lymphoid tissues. Our understanding of the factors that regulate the anatomical program followed by antigen-specific T cells during an infection remains incomplete. Egress of effector T cell from the draining lymph node (dLN) is one of the essential steps for the eventual eradication of the pathogen at the infection site. Although it is known that sphingosine-1-phosphate receptor 1 (S1PR1) controls naive T cell exit, how S1PR1 influences the emigration of effector T cells after infection is not well understood. Herein, by using both in-situ major histocompatibility complex (MHC)-tetramer staining and intravital imaging of a granzyme B (GzmB) YFP reporter mouse, we mapped the endogenous antigen-specific CD8 T cell response after localized viral infection in the dLN. In fact, we observed the localization of effector T cells in the paracortex early after infection, followed by the migration to the periphery. Notably, they exit the dLN via the medullary and cortical lymphatic sinuses. Furthermore, to assess the role of S1PR1 in their dynamic behavior, we generated a conditional GzmB YFP deficient mice to disrupt S1PR1 signals specifically and temporally in effector CD8 T cells after infection. Using this unique model we clearly demonstrate that after infection, even in the absence of retention signals such as CCR7 and CD62L S1PR1 signaling is the overriding factor that regulates effector T cell emigration from the dLN
Chollat-Namy, Marie. "Effet de l’inactivation du gène suppresseur de tumeur p53 et de sa réactivation pharmacologique sur la réponse cytotoxique anti-tumorale The Pharmalogical Reactivation of p53 Function Improves Breast Tumor Cell Lysis by Granzyme B and NK Cells Through Induction of Autophagy Mutant P53 Gain of Function Stimulates PD-L1 Expression". Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL032.
Pełny tekst źródłaImmune system plays an important role in the control and destruction of cancer cells. The major effectors of antitumor immune response are Natural Killer (NK) cells and the cytotoxic T lymphocytes, which recognize et destroy tumor cells by exocytosis of perforin and granzymes contained in cytotoxic granules. It has been previously shown in the laboratory that the tumor suppressor p53 plays an important role in this apoptotic pathway. However more than 50% of human tumors have p53 inactivating mutations which favor tumor development. Consequently, frequent p53 inactivation in human tumor could enable them to escape from destruction by cytotoxic immune cells. In this context, my thesis work has shown that the pharmacological reactivation of wild type p53 function in cancer cells expressing a mutated p53 increased their susceptibility to NK cell-mediated apoptosis cells through the induction of an autophagic process. Moreover, I tried to determine the link between p53 mutations and the expression of the immune checkpoint ligand PD-L1 which prevent efficient activation of cytotoxic cells and promote immune cells exhaustion. My work suggests that the expression of p53 mutants promotes an the expression of PD-L1 at the cancer cell surface. The study of the underlying mechanisms is still in progress
Musembi, Susan Mbithe. "Immunological assays relevant to definition of bovine theileria parva-specific cytotoxic CD8+ T cell responses". Thesis, Brunel University, 2012. http://bura.brunel.ac.uk/handle/2438/7171.
Pełny tekst źródłaCzęści książek na temat "Granzymes"
Greenberg, A. H., i D. W. Litchfield. "Granzymes and Apoptosis: Targeting the Cell Cycle". W Pathways for Cytolysis, 95–119. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79414-8_6.
Pełny tekst źródłaHaddad, Patrick, Dieter E. Jenne, Olivier Krähenbühl i Jürg Tschopp. "Structure and Possible Functions of Lymphocyte Granzymes". W Cytotoxic Cells: Recognition, Effector Function, Generation, and Methods, 251–62. Boston, MA: Birkhäuser Boston, 1993. http://dx.doi.org/10.1007/978-1-4684-6814-4_23.
Pełny tekst źródłaNoonan, Janis, i Brona M. Murphy. "Cytotoxic T Lymphocytes and Their Granzymes: An Overview". W Resistance to Targeted Anti-Cancer Therapeutics, 91–112. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17807-3_5.
Pełny tekst źródłaKuppili, Raja Reddy, i Kakoli Bose. "Calpains and Granzymes: Non-caspase Proteases in Cell Death". W Proteases in Apoptosis: Pathways, Protocols and Translational Advances, 53–94. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19497-4_3.
Pełny tekst źródłaJenne, D. E., i J. Tschopp. "Granzymes: a Family of Serine Proteases in Granules of Cytolytic T Lymphocytes". W Current Topics in Microbiology and Immunology, 33–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73911-8_4.
Pełny tekst źródłaCoughlin, Paul, Emma Morris i Lynne Hampson. "The role of granzymes and serpins in regulating cell growth and death". W Programmed Cell Death in Animals and Plants, 55–64. London: Garland Science, 2021. http://dx.doi.org/10.1201/9781003076889-5.
Pełny tekst źródłaGooch, Jan W. "Granzyme". W Encyclopedic Dictionary of Polymers, 896. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13866.
Pełny tekst źródłaGressner, A. M., i O. A. Gressner. "Granzyme". W Springer Reference Medizin, 1027. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1332.
Pełny tekst źródłaGressner, A. M., i O. A. Gressner. "Granzyme". W Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_1332-1.
Pełny tekst źródłaLeón, Diego López, Isabelle Fellay, Pierre-Yves Mantel i Michael Walch. "Killing Bacteria with Cytotoxic Effector Proteins of Human Killer Immune Cells: Granzymes, Granulysin, and Perforin". W Methods in Molecular Biology, 275–84. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6673-8_18.
Pełny tekst źródłaStreszczenia konferencji na temat "Granzymes"
Ngan, DA, SV Vickerman, PR Hiebert, H. Zhao, WM Elliott, JC Hogg, DJ Granville, SP Man i DD Sin. "The Role of Granzyme B in the Pathogenesis of COPD." W 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.a2961.
Pełny tekst źródłaWiles, Andrew, Claire Hoptay, Matthew Sharron, Mayya Geha, Kanneboyina Nagaraju i Robert J. Freishtat. "Sepsis-Related Mortality Is Reduced In The Absence Of Granzyme B". W American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4677.
Pełny tekst źródłaVickerman, SV, H. Zhao, Y. Li, DA Ngan, PR Hiebert, DJ Granville, SF Man i DD Sin. "Characterization of Granzyme B Protein Expression in Blood from COPD Patients." W 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.a2941.
Pełny tekst źródłaSharron, Matthew, Andrew A. Wiles, Angela S. Benton i Robert J. Freishtat. "Mechanisms Of Platelet Granzyme B Induced End-Organ Apoptosis In Sepsis". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6151.
Pełny tekst źródłaXu, L., F. Hu, X. Liu, L. Zhu, L. Ren, H. Liu, H. Zhu i Y. Su. "AB0102 Impairment of granzyme b-producing regulatory b cells exacerbated rheumatoid arthritis". W Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.2269.
Pełny tekst źródłaSharron, Matthew, Andrew A. Wiles, Claire E. Hoptay, Kanneboyina Nagaraju i Robert J. Freishtat. "Platelet Granzyme B Induces Contact-Dependent End-Organ Apoptosis During Murine Sepsis". W 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.a6009.
Pełny tekst źródłaKim, Won Dong, Kang Hyeon Choe, Yeon Mok Oh, Sang Do Lee, Kyu Rae Kim, Hyun Sook Chi i James C. Hogg. "Granzyme B Positive Cells Outnumber CD8+ Cells In Small Airways Of Centrilobular Emphysema". W American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5803.
Pełny tekst źródłaBarczyk, A., E. Sozanska i W. Pierzchala. "Increased Expression of Granzyme B, but Not Perforin in CD8+ Cells in Sarcoidosis." W 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.a3185.
Pełny tekst źródłaWroblewski, Mark A., Raimund Bauer, Miguel Cubas Córdova, Florian Udonta, Isabel Ben Batalla, Victoria Gensch, Stefanie Sawall i in. "Abstract 3253: Mast cell-derived granzyme b contributes to resistance against anti-angiogenic therapy". W Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3253.
Pełny tekst źródłaShevtsov, Maxim, Susanne Kaesler, Stefan Stangl, Luidmila Yakovleva, Ruslana Tagaeva, Yaroslav Marchenko, Boris Nikolaev i in. "Abstract 2878: Granzyme B functionalized nanocarriers targeting membrane-bound Hsp70 for multimodal cancer therapies". W Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2878.
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