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Inducible resistance to Fas-mediated apoptosis in B cells Rothstein TLCell Res 2000[Dec]; 10 (4): 245-66Apoptosis produced in B cells through Fas (APO-1, CD95) triggering is regulated by signals derived from other surface receptors: CD40 engagement produces upregulation of Fas expression and marked susceptibility to Fas-induced cell death, whereas antigen receptor engagement, or IL-4R engagement, inhibits Fas killing and in so doing induces a state of Fas-resistance, even in otherwise sensitive, CD40-stimulated targets. Surface immunoglobulin and IL-4R utilize at least partially distinct pathways to produce Fas-resistance that differentially depend on PKC and STAT6, respectively. Further, surface immunoglobulin signaling for inducible Fas-resistance bypasses Btk, requires NF-kappaB, and entails new macromolecular synthesis. Terminal effectors of B cell Fas-resistance include the known anti-apoptotic gene products, Bcl-xL and FLIP, and a novel anti-apoptotic gene that encodes FAIM (Fas Apoptosis Inhibitory Molecule). faim was identified by differential display and exists in two alternatively spliced forms; faim-S is broadly expressed, but faim-L expression is tissue-specific. The FAIM sequence is highly evolu- tionarily conserved, suggesting an important role for this molecule throughout phylogeny. Inducible resistance to Fas killing is hypothesized to protect foreign antigen-specific B cells during potentially hazardous interactions with FasL-bearing T cells, whereas autoreactive B cells fail to become Fas-resistant and are deleted via Fas-dependent cytotoxicity. Inadvertent or aberrant acquisition of Fas-resistance may permit autoreactive B cells to escape Fas deletion, and malignant lymphocytes to impede anti-tumor immunity.|*Intracellular Signaling Peptides and Proteins[MESH]|*Signal Transduction[MESH]|Agammaglobulinaemia Tyrosine Kinase[MESH]|Animals[MESH]|Apoptosis/*physiology[MESH]|B-Lymphocytes/*physiology[MESH]|CASP8 and FADD-Like Apoptosis Regulating Protein[MESH]|CD40 Antigens/metabolism[MESH]|CD40 Ligand/metabolism[MESH]|Carrier Proteins/genetics/metabolism[MESH]|Humans[MESH]|NF-kappa B/metabolism[MESH]|Protein Kinase C/metabolism[MESH]|Protein-Tyrosine Kinases/metabolism[MESH]|Proto-Oncogene Proteins c-bcl-2/genetics/metabolism[MESH]|bcl-X Protein[MESH]|fas Receptor/genetics/*metabolism[MESH] |
