PubMed:10229231 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PubMed/sourceid/10229231","sourcedb":"PubMed","sourceid":"10229231","source_url":"http://www.ncbi.nlm.nih.gov/pubmed/10229231","text":"Regulation of Fas ligand expression and cell death by apoptosis-linked gene 4.\nProgrammed cell death is a process required for the normal development of an organism. One of the best understood apoptotic pathways occurs in T lymphocytes and is mediated by Fas/Fas ligand (FasL) interaction. During studies of apoptosis induced by T cell-receptor engagement, we identified ALG-4F, a truncated transcript that prevents T cell-receptor-induced FasL upregulation and cell death. Overexpression of full-length ALG-4 induced transcription of FasL and, consequently, apoptosis. These results indicate that ALG-4 is necessary and sufficient for FasL expression. Fas/FasL interaction initiates cell death in many other systems, and its dysregulation is a mechanism by which several pathologic conditions arise. Understanding the molecular mechanisms of FasL regulation could be very useful in elucidating how these diseases develop and in identifying potential therapeutic 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