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Academic literature on the topic 'Signalisation du BCR'
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Journal articles on the topic "Signalisation du BCR"
Deglesne, Pierre-Antoine, Natalie Chevallier, Remi Letestu, Celia Salanoubat, Laurence Sanhes, Joelle Nataf, Nadine Varin-Blank, and Florence Ajchenbaum-Cymbalista. "B Cell Receptor (BCR) Ligation Enhances Cell Survival in Progressive Chronic Lymphocytic Leukemia (CLL)." Blood 104, no. 11 (November 16, 2004): 966. http://dx.doi.org/10.1182/blood.v104.11.966.966.
Full textDissertations / Theses on the topic "Signalisation du BCR"
Kheirallah, Samar. "Implication de la signalisation du BCR dans le ciblage thérapeutique des lymphomes folliculaires." Toulouse 3, 2010. http://thesesups.ups-tlse.fr/1259/.
Full textBeside its central role in the recognition of antigen, the BCR (B Cell Receptor) controls a multitude of intracellular mechanisms that regulate B lymphocyte biology. Altered BCR signaling has been demonstrated in various types of B-cell lymphoma and some autoimmune diseases. Thus, therapeutic targeting of BCR signaling has been the focus of my PhD studies. We demonstrate that the monoclonal anti-CD20 antibody, Rituximab, inhibits BCR signaling at least by down-regulating BCR expression. Furthermore, enzastaurin (kinases inhibitor) exerts an anti-tumoral effect on follicular lymphoma cells by inhibiting downstream BCR signaling. Then, we characterized new mechanisms of action of Rituximab and enzastaurin and we focused on the importance of BCR signaling in lymphoma's therapy
Malissein, Emilie. "Physiologie mitochondriale et apoptose couplée à la signalisation du récepteur à l'antigène des lymphocytes B." Limoges, 2005. http://aurore.unilim.fr/theses/nxfile/default/d34a6617-a544-4cab-8d1a-a6725a6a863f/blobholder:0/2005LIMO0009.pdf.
Full textBCR signaling presents differential functional responses, dependent of B cell stage of differentiation. The pro-apoptotic activity of Bad protein and its intracellular traffic are regulated by phosphorylation and dephosphorylation. Modulation of Bad phosphorylation during BCR-induced apoptosis and correlation with cell death mitochondrial pathway are not fully characterized. We show by flow cytometry, immunoprecipitation, Western Blotting and confocal microscopy that : (i) Bad activation (dephosphorylation) is implicated in BCR-induced apoptosis of immature B lymphocytes (ii) regulation of Bad phosphorylation status may contribute to BCR functional duality (survival/apoptosis) (iii) differential subcellular compartmentalization of Bad (in particular in rafts) may contribute to sensitize immature B cells to apoptosis
Amin, Ali Rada. "BCR de classe IgA : signalisation de la cellule B normale et dans un contexte de lymphoprolifération." Limoges, 2009. http://www.theses.fr/2009LIMO4069.
Full textIn order to map new QTL regulating male fertility parameter, we analysed a set of Interspecific Recombinant Congenic strain. We mapped 8 QTL implicated in testis, development, prostate growth, sperm vitality and morphology. We performed fine mapping analysis of a QTL of reduced testis weight associated with teratozoospermia, localised on MMU11. We proposed a candidate locus encompassing four testis expressed gene. Moreover, in order to understand gene expression regulation in interspecific mosaic genome, we analysed testis transcriptome of three IRC strains compared with parental strains testis transcriptome. In this study, we describe how spretus genes are regulated when introgressed in musculus background. This study gives some insight concerning gene flow tolerance across the specie barrier during emergence of mosaic genome
Harouna, Rachidi Abdou Souleymane. "Etudes structurale et fonctionnelle de la protéine Syk dans les cellules B de Leucémie Lymphoïde Chronique." Electronic Thesis or Diss., Paris 13, 2024. http://www.theses.fr/2024PA131024.
Full textChronic Lymphocytic Leukemia (CLL) has a variable clinical course, with some patients remaining stable while others experience progression. By stimulating the B Cell Receptor (BCR) in CLL B cells ex-vivo, it is possible to distinguish between non-responder (NR) and responder (R) cases based on cell survival. This survival rate correlates with overall patient survival. Differential phosphorylation levels of Syk, a key kinase in BCR signaling, suggest that post-translationally modified Syk contributes to CLL progression. Our studies reveal differences in global and specific phosphorylation kinetics and spot patterns of Syk between CLL B cells in basal and BCR-stimulated conditions, arguing for the dedicated role of Syk-specific sites. Functional analysis of Syk phosphorylation mutants targeting its activation process or its ability to bind partners shows their distinct involvement in metabolic activity, cytokine secretion, and signaling pathways upon BCR activation. Collectively, our findings provide new insights into the potential role of Syk conformation in CLL pathogenesis and offer insights into potential therapeutic targets for the disease
Rochelle, Tristan. "Signalisation des GTPases de la famille Rho dans les phénotypes migratoires induits par les différentes formes de Bcr-Abl." Thesis, Poitiers, 2012. http://www.theses.fr/2012POIT1401/document.
Full textBcr-Abl chimeric oncogenes (p190bcr-abl and p210bcr-abl) result from the t(9,22) chromosomal translocation that fuse the bcr and the c-abl genes. p210bcr-abl and p190bcr-abl are associated with Chronic Myelogenous Leukemia (CML) and a subset of Acute Lymphoblastic Leukemia (ALL) respectively. The only difference between these two chimeras is the presence of a specific RhoA-GEF domain in the p210bcr-abl oncogene. Bcr-Abl expression in Ba/F3 lymphoblasts induces spontaneous migration of these cells without apparent directionality. Motility triggering of Bcr-Abl-expressing Ba/F3 depends on the RhoGTPase Rac1.RhoA activity is associated with a typical amoeboid movement of Ba/F3p210 cells embedded in Matrigel™ 3D matrix, whereas the Ba/F3p190 cells, devoid of RhoA activity, display a rolling-type motility. In this work we showed that activation of the RhoA effector ROCK1 triggers two parallel pathways which are both necessary for amoeboid movement: 1) the Myosin Light chain (MLC) pathway 2) ADF family proteins (Actin Depolymerizing Factor) pathway, specifically the ADF/destrin isoform. Besides, we showed that Ba/F3p190 cells could assemble invadopodia-like structures. The formation of these structures is driven by the reduction of RhoA activity associated with the absence of the DH/PH domain in p190bcr-abl and correlates with an increase in Cdc42 activity. We finally demonstrated that the RhoA/ROCK pathway is constitutively activated in CD34+ cells isolated from CML patients while not in their normal counterparts. We also demonstrated that this activation is independent of the tyrosine Kinase activity of Bcr-Abl
Aouar, Besma. "Altération de la production d'interféron de type I par les cellules plasmacytoïdes dendritiques : ciblage de la voie de signalisation BCR-like." Thesis, Aix-Marseille, 2015. http://www.theses.fr/2015AIXM5021.
Full textPlasmacytoid dendritic cells are major producers of type I IFN in human organism. During chronic viral infections, such as Hepatitis C Virus infection, pDCs are functionally impaired. More than 50% efficiency of IFN-α treatment, until recently used, suggested that modulation of pDC function could be an important target for HCV treatment. pDCs recognize HCV RNA by Toll-like receptors, and dispose of a set of so-called regulatory receptors that regulate IFN-I production. Crosslinking of these RR such as BDCA-2 and ILT7 has been shown to inhibit IFN-I production by pDCs stimulated with TLR7/9 agonists. In this work we show that HCV envelope glycoprotein E2 is a novel ligand of pDC RR, BDCA-2 and DCIR, and that this binding is responsible for IFN-I inhibition via the activation of the BCR-like pathway. Then we assayed to restore IFN-I in pDCs with crosslinked RR by targeting well-known kinases of BCR-like pathway, Syk and Mek. When inhibiting Syk, IFN-I was only partially restored by subliminal concentrations of Syk inhibitor; high concentrations of Syk inhibitor effectively blocked IFN-I production, suggesting involvement of Syk in the TLR7/9 pathway as it was already demonstrated in TLR activation in macrophages. When inhibiting MEK, the restoration of type I IFN was effective. The underlying mechanisms leading to the restoration are further explored. Pharmacological targeting of BCR-like signaling may constitute an attractive new approach to study mechanisms of modulation of pDC activation in pathophysiological conditions
Louat, Thierry. "Signalisation et (in)stabilité génétique : nouvelles voies de régulation de la réparation de l'ADN." Toulouse 3, 2004. http://www.theses.fr/2004TOU30102.
Full textCells and DNA are exposed to various endogenous or exogenous genotoxic insults. Cells dispose of six DNA repair mechanisms. Among these, the nucleotide excision repair, NER, corrects a large variety of damage. We focused on the impact of kinase expression, p210BCR-ABL and PKCzeta, in DNA repair activity modulation. P210bcr-abl oncogene transfection in myeloid cells increases NER activity in a kinase activity-dependant pathway. Inversely, p210BCR-ABL expression in a lymphoid cell line represses NER activity and sensitises cells to UVC in a kinase activity-dependant pathway. P210BCR-ABL seems to target the initial steps of the NER process, before XPB recruitment occurs. We also show that ectopic expression of PKCzeta confers cell resistance to UVC, cisplatin and melphalan. PKCzeta overexpression stimulates NER activity by increasing global genome repair and transcription-coupled repair detection complex levels. CSA and CSB proteins are overexpressed by Sp1-mediated transcriptional stimulation. Reasons for XPC/hHR23B overexpression were unable to be elucidated thought transcriptional and direct phosphorylation, however are excluded. PKCzeta interacts with, and phosphorylates, the mismatch detection complex, hMutSalpha. Its phosphorylation prohibits proteasome degradation and increases mismatch repair activity. .
Bourgeais, Jérôme. "Fonctions oncogéniques de STAT5 : rôle dans la régulation du métabolisme oxydatif." Thesis, Tours, 2015. http://www.theses.fr/2015TOUR4051.
Full textThe Signal Transducer and Activator of Transcription factors 5A and B are two closely related STAT family members that play a major role in normal and leukemic hematopoiesis. STAT5 proteins are frequently activated in hematopoietic neoplasms and are targets of various tyrosine kinase oncogenes such as BCR-ABL and JAK2V617F. Both oncogenes were shown to stimulate the production of intracellular ROS (Reactive Oxygen Species) in leukemic cells and evidences for a cross talk between STAT5 and ROS metabolism have recently emerged. Herein, we demonstrate that sustained activation of STAT5 induced by BCR-ABL promotes ROS production in Chronic Myeloid Leukemia (CML) cells by repressing expression of two antioxidants, catalase and glutaredoxin1 and by possible functional interactions with NADPH oxidase complexes. We also provide compelling evidences that tyrosine phosphorylation regulate the pro-oxidant activity of STAT5 and that non phosphorylated STAT5 displays antioxidant properties and protection against oxidative stress via non-genomic effects. This dual function of STAT5 is also illustrated in an in vitro microenvironment model that we develop in our laboratory to analyze interactions between bone marrow stromal cells and CML cells. Using these coculture experiments, we show that STAT5 phosphorylation was reduced and its antioxidant activity enhanced in leukemic cells in contact with stromal cells. We also demonstrate in this model that leukemic cells stopped dividing, entered a quiescent G0 state and became resistant to Imatinib, a BCR-ABL kinase inhibitor. Collectively, these findings suggest an important link between antioxidant activity of STAT5, quiescence and resistance to chemotherapeutic agents in leukemic cells
Fournier, Emilie. "Régulation positive et négative de l'activation des lymphocytes B humains normaux et pathologiques." Paris 6, 2008. http://www.theses.fr/2008PA066150.
Full textNicolle, Delphine. "Implication des voies de signalisation Toll (TLR) dans la réponse immunitaire aux mycobactéries." Orléans, 2004. http://www.theses.fr/2004ORLE2043.
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