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Science 3 October 1997:
Vol. 278. no. 5335, pp. 138 - 141
DOI: 10.1126/science.278.5335.138

Reports

NF-AT Activation Induced by a CAML-Interacting Member of the Tumor Necrosis Factor Receptor Superfamily

Götz-Ulrich von Bülow, Richard J. Bram *

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

G.-U. von Bülow, Department of Experimental Oncology, St. Jude Children's Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA.
R. J. Bram, Departments of Experimental Oncology and Hematology/Oncology, St. Jude Children's Research Hospital, 332 North Lauderdale, and Department of Pediatrics, University of Tennessee, Memphis, TN 38105, USA.
*   To whom correspondence should be addressed. E-mail: richard.bram{at}stjude.org

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