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

Götz Ulrich Von Bülow, Richard J Bram

Research output: Contribution to journalArticle

282 Citations (Scopus)

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 TACl-specific antibodies led to activation of the transcription factors NF-AT, AP-1, and NFκB. TACl-induced activation of NF- AT was specifically blocked by a dominant-negative CAML mutant, thus implicating CAML as a signaling intermediate.

Original languageEnglish (US)
Pages (from-to)138-141
Number of pages4
JournalScience
Volume278
Issue number5335
DOIs
StatePublished - Oct 3 1997
Externally publishedYes

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Cyclophilins
Tumor Necrosis Factor Receptors
NFATC Transcription Factors
Ligands
Calcium
Jurkat Cells
Lymphocytes
TCF Transcription Factors
Transcription Factor AP-1
Proteins
T-Lymphocytes
Antibodies

ASJC Scopus subject areas

  • General

Cite this

NF-AT activation induced by a CAML-interacting member of the tumor necrosis factor receptor superfamily. / Von Bülow, Götz Ulrich; Bram, Richard J.

In: Science, Vol. 278, No. 5335, 03.10.1997, p. 138-141.

Research output: Contribution to journalArticle

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