PubMed:9311921 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PubMed/sourceid/9311921","sourcedb":"PubMed","sourceid":"9311921","source_url":"http://www.ncbi.nlm.nih.gov/pubmed/9311921","text":"NF-AT activation induced by a CAML-interacting member of the tumor necrosis factor receptor superfamily.\nActivation of the nuclear factor of activated T cells transcription factor (NF-AT) is a key event underlying lymphocyte action. The CAML (calcium-modulator and cyclophilin ligand) protein is a coinducer of NF-AT activation when overexpressed in Jurkat T cells. A member of the tumor necrosis factor receptor superfamily was isolated by virtue of its affinity for CAML. Cross-linking of this lymphocyte-specific protein, designated TACI (transmembrane activator and CAML-interactor), on the surface of transfected Jurkat cells with TACI-specific antibodies led to activation of the transcription factors NF-AT, AP-1, and NFkappaB. 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