期刊
SCIENCE
卷 316, 期 5825, 页码 754-758出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1137895
关键词
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资金
- NIAID NIH HHS [F32 AI063793-01A1, R01AI056016, F32AI063793, R01AI038474, F32 AI063793] Funding Source: Medline
- NIDCR NIH HHS [T32DE007288] Funding Source: Medline
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-kappa B. Stimulation of ADAP-deficient mouse T cells with antibodies to CD3 and CD28 resulted in impaired nuclear translocation of NF-kappa B, a reduced DNA binding, and delayed degradation and decreased phosphorylation of I kappa B ( inhibitor of NF-kappa B). 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 association with the CARMA1 adapter and NF-kappa B activation but is not required for ADAP-dependent regulation of adhesion. These findings provide new insights into ADAP function and the mechanism by which CARMA1 regulates NF-kappa B activation in T cells.
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