布鲁顿酪氨酸激酶
B细胞受体
B细胞
断点群集区域
酪氨酸激酶
细胞生物学
受体
细胞
癌症研究
生物
信号转导
免疫学
抗体
遗传学
作者
Anne B. Satterthwaite,Zuomei Li,Owen N. Witte
标识
DOI:10.1006/smim.1998.0123
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+ flux, activating JNK and p38 and inducing cell cycle regulatory genes.
科研通智能强力驱动
Strongly Powered by AbleSci AI