TY - JOUR
T1 - NF-AT activation induced by a CAML-interacting member of the tumor necrosis factor receptor superfamily
AU - Von Bülow, Götz Ulrich
AU - Bram, Richard J.
PY - 1997/10/3
Y1 - 1997/10/3
N2 - 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.
AB - 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.
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U2 - 10.1126/science.278.5335.138
DO - 10.1126/science.278.5335.138
M3 - Article
C2 - 9311921
AN - SCOPUS:0039792391
SN - 0036-8075
VL - 278
SP - 138
EP - 141
JO - Science
JF - Science
IS - 5335
ER -