期刊
JOURNAL OF IMMUNOLOGY
卷 191, 期 12, 页码 6208-6221出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1301587
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资金
- American Heart Association [11PRE7390070]
- National Institutes of Health [T32AI007485, R01 CA136729]
- American Heart Association Scientist Development [0830244N]
Focal adhesion kinase (FAK) is a critical regulator of signal transduction in multiple cell types. Although this protein is activated upon TCR engagement, the cellular function that FAK plays in mature human T cells is unknown. By suppressing the function of FAK, we revealed that FAK inhibits TCR-mediated signaling by recruiting C-terminal Src kinase to the membrane and/or receptor complex following TCR activation. Thus, in the absence of FAK, the inhibitory phosphorylation of Lck and/or Fyn is impaired. Together, these data highlight a novel role for FAK as a negative regulator TCR function in human T cells. These results also suggest that changes in FAK expression could modulate sensitivity to TCR stimulation and contribute to the progression of T cell malignancies and autoimmune diseases.
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