SHIP modulates immune receptor responses by regulating membrane association of Btk

被引：325

作者：

Bolland, S

Pearse, RN

Kurosaki, T

Ravetch, JV ^{[1
]}

机构：

[1] Rockefeller Univ, Lab Mol Genet & Immunol, New York, NY 10021 USA

[2] Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10021 USA

[3] Kansai Med Univ, Dept Mol Genet, Moriguchi, Osaka 570, Japan

来源：

IMMUNITY | 1998年 / 8卷 / 04期

基金：

美国国家卫生研究院;

关键词：

D O I：

10.1016/S1074-7613(00)80555-5

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Membrane recruitment of SHIP is responsible for the inhibitory signal generated by Fc gamma RIIB coligation to the BCR. By reducing the level of PIP3, SHIP regulates the association of the tyrosine kinase Btk with the membrane through PH domain-phosphoinositol lipid interactions. Inhibition of BCR signaling by either Fc gamma RIIB coligation, membrane expression of SHIP, or inhibition of PI3K, conditions which result in decreased levels of PIP3, is suppressed by the expression of Btk as a membrane-associated chimera. Conversely, increasing PIP3 levels by deletion of SHIP results in increased Btk association with the membrane and hyperresponsive BCR signaling. These results suggest a central role for PIP3 in regulating the B cell stimulatory state by modulating Btk localization and thereby calcium fluxes.

引用

收藏

页码：509 / 516

页数：8

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