Btk function in B cell development and response

被引:161
作者
Satterthwaite, AB [1 ]
Li, ZM
Witte, ON
机构
[1] Univ Calif Los Angeles, Dept Microbiol & Mol Genet, Los Angeles, CA 90095 USA
[2] Univ Calif Los Angeles, Howard Hughes Med Inst, Los Angeles, CA 90095 USA
关键词
B cell antigen receptor (BCR); Bruton's tyrosine kinase (Btk); immunodeficiency; pleckstrin homology (PH) domain; tyrosine phosphorylation;
D O I
10.1006/smim.1998.0123
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Mutations in Bruton's tyrosine kinase (Btk) result in the B cell immunodeficiencies XLA in humans and Xid in mice. Both the maintenance of peripheral B cell numbers and their response to B cell antigen receptor (BCR) crosslinking depend on Btk. Btk integrates signals from multiple cell surface receptors, including BCR and G-protein coupled receptors. These Btk dependent signals control B cell proliferation and survival by mediating Ca2+ pus activating JNK and p38 and inducing cell cycle regulatory genes.
引用
收藏
页码:309 / 316
页数:8
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