Activation of BTK by a phosphorylation mechanism initiated by SRC family kinases

被引:396
作者
Rawlings, DJ
Scharenberg, AM
Park, H
Wahl, MI
Lin, SQ
Kato, RM
Fluckiger, AC
Witte, ON
Kinet, JP
机构
[1] BETH ISRAEL HOSP, LAB ALLERGY & IMMUNOL, BOSTON, MA 02215 USA
[2] HARVARD UNIV, SCH MED, BOSTON, MA 02215 USA
[3] UNIV CALIF LOS ANGELES, DEPT MICROBIOL & MOLEC GENET, LOS ANGELES, CA 90095 USA
[4] UNIV CALIF LOS ANGELES, HOWARD HUGHES MED INST, LOS ANGELES, CA 90095 USA
[5] UNIV CALIF LOS ANGELES, INST MOLEC BIOL, LOS ANGELES, CA 90095 USA
关键词
D O I
10.1126/science.271.5250.822
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Bruton's tyrosine kinase (BTK) is pivotal in B cell activation and development through its participation in the signaling pathways of multiple hematopoietic receptors. The mechanisms controlling BTK activation were studied here by examination of the biochemical consequences of an interaction between BTK and SRC family kinases. This interaction of BTK with SRC kinases transphosphorylated BTK on tyrosine at residue 551, which led to BTK activation. BTK then autophosphorylated at a second site. The same two sites were phosphorylated upon B cell antigen receptor cross-linking. The activated BTK was predominantly membrane-associated, which suggests that BTK integrates distinct receptor signals resulting in SRC kinase activation and BTK membrane targeting.
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页码:822 / 825
页数:4
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