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Regulation of NF-KB Activation in T Cells via Association of the Adapter Proteins ADAP and CARMA1
Oleh:
Medeiros, Ricardo B.
;
Burbach, Brandon J
;
Mueller, Kristen L.
;
Srivastava, Rupa
;
Moon, James J.
;
Highfill, Sarah
;
peterson, Erik J.
;
Shimizu, Yoji
Jenis:
Article from Bulletin/Magazine
Dalam koleksi:
SCIENCE (keterangan: ada di Proquest) vol. 316 no. 5825 (May 2007)
,
page 754.
Topik:
Immunology
Ketersediaan
Perpustakaan FK
Nomor Panggil:
S01.K.2007.05
Non-tandon:
1 (dapat dipinjam: 0)
Tandon:
tidak ada
Lihat Detail Induk
Isi artikel
The adapter protein ADAP regulates T lymphocyte adhesion and activation. We present evidence for a previously unrecognized function for ADAP in regulating T .cell receptor (TCR)-mediated activation of the transcription factor NF-KB. Stimulation of ADAP-defident mouse T cells with antibodies to CD3 and CD28 resulted in impaired nuclear translocation of NF-KB, a reduced DNA binding, and delayed degradation and decreased phosphorylation of IKB (inhibitor of NF-KB). TCR-stimulated assembly of the CARMA1-BCL-10-MALT1 complex was substantially impaired in the absence of ADAP. We further identified a region of ADAP that is required for assodation with the CARMA1 adapter and NF-KB activation but is not required for ADAP-dependent regulation of adhesion. These findings provide new insights into ADAP function and the mechanism by which CARMAlregulates NF-KB activation in T cells.
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