Involvement of LAT, Gads, and Grb2 in compartmentation of SLP-76 to the plasma membrane.

Involvement of LAT, Gads, and Grb2 in compartmentation of SLP-76 to the plasma membrane.
复制标题

DOI:
10.1084/jem.192.6.847
复制
发表时间:
2000-09-18
期刊:
The Journal of experimental medicine
影响因子:
--
通讯作者:
Kurosaki T
Kurosaki T
中科院分区:
其他
文献类型:
--
作者:
Ishiai M;Kurosaki M;Inabe K;Chan AC;Sugamura K;Kurosaki T

文献摘要

参考文献

被引文献

相似文献

B细胞连接蛋白(BLNK)和76 kD的含Src同源2结构域的白细胞蛋白(SLP-76)分别是B细胞受体(BCR)和T细胞受体功能所需的衔接蛋白。在这里,我们发现SLP-76的表达不能重建Zap-70+BLNK− B细胞中的BCR功能。这可能是由于抗原受体交联后SLP-76不能被募集到富含糖脂的微区(GEM)中。支持这一观点的是,当膜相关的SLP-76嵌合体被强制定位于GEM时,BCR功能恢复。此外,我们证明了向SLP-76添加用于活化T细胞的接头(LAT)和Shc下游的Grb 2相关衔接子(Gads)允许SLP-76被募集到GEM中,由此重建BCR功能。Gads功能能够被Grb 2的过表达所取代。与SLP-76相比,BLNK不需要Grb 2家族来招募GEM。因此,这些数据表明BLNK和SLP-76之间的功能重叠,同时强调了在靶向GEM时对额外衔接子分子的需求的差异。
B cell linker protein (BLNK) and Src homology 2 domain–containing leukocyte protein of 76 kD (SLP-76) are adaptor proteins required for B cell receptor (BCR) and T cell receptor function, respectively. Here, we show that expression of SLP-76 cannot reconstitute BCR function in Zap-70+BLNK− B cells. This could be attributable to inability of SLP-76 to be recruited into glycolipid-enriched microdomains (GEMs) after antigen receptor cross-linking. Supporting this idea, the BCR function was restored when a membrane-associated SLP-76 chimera was enforcedly localized to GEMs. Moreover, we demonstrate that addition of both linker for activation of T cells (LAT) and Grb2-related adaptor downstream of Shc (Gads) to SLP-76 allow SLP-76 to be recruited into GEMs, whereby the BCR function is reconstituted. The Gads function was able to be replaced by overexpression of Grb2. In contrast to SLP-76, BLNK did not require Grb2 families for its recruitment to GEMs. Hence, these data suggest a functional overlap between BLNK and SLP-76, while emphasizing the difference in requirement for additional adaptor molecules in their targeting to GEMs.
DOI: 10.1016/s1074-7613(00)80192-2
发表时间: 2000-04-01
期刊: IMMUNITY
影响因子: 32.4
作者:
Liou, J;Kiefer, F;Weiss, A
通讯作者: Weiss, A
DOI: 10.1016/1074-7613(95)90029-2
发表时间: 1995-05-01
期刊: IMMUNITY
影响因子: 32.4
作者:
KONG, GH;BU, JY;CHAN, AC
通讯作者: CHAN, AC
DOI: 10.1084/jem.189.8.1243
发表时间: 1999-04-19
期刊: The Journal of experimental medicine
影响因子: --
作者:
Law CL;Ewings MK;Chaudhary PM;Solow SA;Yun TJ;Marshall AJ;Hood L;Clark EA
通讯作者: Clark EA
DOI: 10.1016/s0960-9822(99)80017-7
发表时间: 1999-01-28
期刊: CURRENT BIOLOGY
影响因子: 9.2
作者:
Liu, SK;Fang, N;McGlade, CJ
通讯作者: McGlade, CJ
DOI: 10.1016/s1074-7613(00)80591-9
发表时间: 1998-07-01
期刊: IMMUNITY
影响因子: 32.4
作者:
Fu, C;Turck, CW;Chan, AC
通讯作者: Chan, AC