VASCULAR SYSTEM DEFECTS AND NEURONAL APOPTOSIS IN MICE LACKING RAS GTPASE-ACTIVATING PROTEIN
VASCULAR SYSTEM DEFECTS AND NEURONAL APOPTOSIS IN MICE LACKING RAS GTPASE-ACTIVATING PROTEIN
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DOI：
10.1038/377695a0
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发表时间：
1995-10-26
期刊：
影响因子：
64.8
通讯作者：
PAWSON, T
中科院分区：
文献类型：
--
作者：
HENKEMEYER, M;ROSSI, DJ;PAWSON, T
编码p120-rasGAP（pas的负调节因子）的基因已在小鼠中被破坏。这种Gap突变影响内皮细胞组织成高度血管化网络的能力，并导致广泛的神经元细胞死亡。差距和Nf 1基因的突变具有协同效应，使得两种基因突变的纯合子胚胎显示出加重的Gap表型。因此，rasGAP和神经纤维蛋白在胚胎发育过程中共同调节pas活性。
The gene encoding p120-rasGAP, a negative regulator of pas, has been disrupted in mice. This Gap mutation affects the ability of endothelial cells to organize into a highly vascularized network and results in extensive neuronal cell death. Mutations in the Gap and Nf1 genes have a synergistic effect, such that embryos homozygous for mutations in both genes show an exacerbated Gap phenotype. Thus rasGAP and neurofibromin act together to regulate pas activity during embryonic development.