Requirement for B cell linker protein (BLNK) in B cell development

被引：242

作者：

Pappu, R

Cheng, AM

Li, B

Gong, Q

Chiu, C

Griffin, N

White, M

Sleckman, BP

Chan, AC ^{[1
]}

机构：

[1] Washington Univ, Sch Med, Ctr Immunol, St Louis, MO 63110 USA

[2] Washington Univ, Sch Med, Div Rheumatol, St Louis, MO 63110 USA

[3] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA

[4] Washington Univ, Sch Med, Dept Pathol, St Louis, MO 63110 USA

[5] Washington Univ, Sch Med, Howard Hughes Med Inst, St Louis, MO 63110 USA

来源：

SCIENCE | 1999年 / 286卷 / 5446期

关键词：

D O I：

10.1126/science.286.5446.1949

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：

Linker proteins function as molecular scaffolds to Localize enzymes with substrates. In B cells, B cell Linker protein (BLNK) Links the B cell receptor (BCR)activated Syk kinase to the phosphoinositide and mitogen-activated kinase pathways. To examine the in vivo role of BLNK, mice deficient in BLNK were generated. B cell development in BLNK-/- mice was blocked at the transition from B220(+) CD43(+) progenitor B to B220(+) CD43(-) precursor B cells. Only a small percentage of immunoglobulin M++ (IgM(++)), but not mature IgM(lo)lgD(hi), B cells were detected in the periphery. Hence, BLNK is an essential component of BCR signaling pathways and is required to promote B cell development.

引用

页码：1949 / 1954

页数：6

共 37 条

[1] DEFECTIVE T-CELL RECEPTOR SIGNALING AND CD8(+) THYMIC SELECTION IN HUMANS LACKING ZAP-70 KINASE [J].