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Science. 1997 Oct 3;278(5335):138-41.

NF-AT activation induced by a CAML-interacting member of the tumor necrosis factor receptor superfamily.

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  • 1Department of Experimental Oncology, St. Jude Children's Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA.

Abstract

Activation 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. TACI-induced activation of NF-AT was specifically blocked by a dominant-negative CAML mutant, thus implicating CAML as a signaling intermediate.

PMID:
9311921
[PubMed - indexed for MEDLINE]
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