Regulation of cytokinesis by mgcRacGAP in B lymphocytes is independent of GAP activity
Regulation of cytokinesis by mgcRacGAP in B lymphocytes is independent of GAP activity
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DOI：
10.1016/j.yexcr.2006.07.026
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发表时间：
2006-11-01
影响因子：
3.7
通讯作者：
Kurosaki, Tomohiro
中科院分区：
文献类型：
--
作者：
Yamada, Takayuki;Hikida, Masaki;Kurosaki, Tomohiro
在细胞分裂中，包括小G蛋白及其调节因子在内的一些分子已知具有重要作用。其中一种调节因子mgcRacGAP对Rac、Cdc42和Rho具有GTPase激活蛋白（GAP）活性。MgcRacGAP也被证明参与各种细胞类型的细胞质分裂。然而，在B淋巴细胞中，mgcRacGAP对细胞分裂和存活的要求尚未得到充分的研究。在这里，我们证明了B淋巴细胞的正常细胞分裂需要GAP和NH2末端结构域，而不需要mgcRacGAP的GAP活性。此外，我们报道了由条件消融mgcRacGAP诱导的B细胞系细胞凋亡通过引入GAP失活突变体而完全恢复，这表明mgcRacGAP缺陷B细胞的存活缺陷也独立于GAP活性。(c) 2006爱思唯尔公司版权所有。
in cytokinesis, several molecules including small G proteins and their regulators are known to have important roles. One of these regulators, mgcRacGAP has GTPase activating protein (GAP) activity for Rac, Cdc42 and Rho. MgcRacGAP has also been shown to be involved in cytokinesis using various cell types. However, the requirement of mgcRacGAP for cytokinesis and survival in B lymphocytes has not been fully examined. Here, we demonstrate that normal cytokinesis in B lymphocytes requires the GAP and NH2 terminal domains but not GAP activity of mgcRacGAP. In addition, we report that apoptosis induced by conditional ablation of mgcRacGAP in the B cell line is fully rescued by the introduction of a GAP-inactive mutant, suggesting that the survival defect in mgcRacGAP-deficient B cells is also independent of GAP activity. (c) 2006 Elsevier Inc. All rights reserved.