PubMed:10229231 JSONTXT

{"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":14,"end":24},"obj":"protein"},{"id":"T2","span":{"begin":54,"end":77},"obj":"DNA"},{"id":"T3","span":{"begin":222,"end":235},"obj":"cell_type"},{"id":"T4","span":{"begin":255,"end":258},"obj":"protein"},{"id":"T5","span":{"begin":258,"end":269},"obj":"protein"},{"id":"T6","span":{"begin":271,"end":275},"obj":"protein"},{"id":"T7","span":{"begin":371,"end":377},"obj":"protein"},{"id":"T8","span":{"begin":381,"end":401},"obj":"protein"},{"id":"T9","span":{"begin":440,"end":444},"obj":"protein"},{"id":"T10","span":{"begin":492,"end":509},"obj":"protein"},{"id":"T11","span":{"begin":535,"end":539},"obj":"protein"},{"id":"T12","span":{"begin":598,"end":603},"obj":"protein"},{"id":"T13","span":{"begin":636,"end":640},"obj":"protein"},{"id":"T14","span":{"begin":657,"end":661},"obj":"protein"},{"id":"T15","span":{"begin":843,"end":847},"obj":"protein"}],"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 targets."}

{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":78},"obj":"Sentence"},{"id":"S2","span":{"begin":79,"end":165},"obj":"Sentence"},{"id":"S3","span":{"begin":166,"end":289},"obj":"Sentence"},{"id":"S4","span":{"begin":290,"end":473},"obj":"Sentence"},{"id":"S5","span":{"begin":474,"end":569},"obj":"Sentence"},{"id":"S6","span":{"begin":570,"end":652},"obj":"Sentence"},{"id":"S7","span":{"begin":653,"end":800},"obj":"Sentence"},{"id":"S8","span":{"begin":801,"end":971},"obj":"Sentence"}],"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 targets."}

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