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