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Involvement of a Small GTP-binding Protein (G Protein) Regulator, Small G Protein GDP Dissociation Stimulator, in Antiapoptotic Cell Survival Signaling

机译:小GTP结合蛋白(G蛋白)调节剂,小G蛋白GDP离解刺激物,参与抗凋亡细胞生存信号传导。

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摘要

Small GTP-binding protein GDP dissociation stimulator (Smg GDS) regulates GDP/GTP exchange reaction of Ki-Ras and the Rho and Rap1 family members and inhibits their binding to membranes. In fibroblasts, Smg GDS shows mitogenic and transforming activities in cooperation with Ki-Ras. However, the physiological function of Smg GDS remains unknown. Here we show that mice lacking Smg GDS died of heart failure shortly after birth, not resulting from developmental heart defects but from enhanced apoptosis of cardiomyocytes triggered by cardiovascular overload. Furthermore, neonatal thymocytes and developing neuronal cells underwent apoptotic cell death. Smg GDS−/− thymocytes were susceptible to apoptotic inducers, such as etoposide and UV irradiation. Smg GDS−/− thymocytes were protected from etoposide-induced cell death by ex vivo transduction of the Smg GDS cDNA. These phenotypes partly coincide with those observed in Ki-Ras-deficient mice, suggesting that Smg GDS is involved in antiapoptotic cell survival signaling through Ki-Ras.
机译:小型GTP结合蛋白GDP解离刺激剂(Smg GDS)调节Ki-Ras和Rho和Rap1家族成员的GDP / GTP交换反应,并抑制它们与膜的结合。在成纤维细胞中,Smg GDS与Ki-Ras合作显示有丝分裂和转化活性。但是,Smg GDS的生理功能仍然未知。在这里,我们显示缺乏Smg GDS的小鼠出生后不久就死于心力衰竭,这不是由心脏发育缺陷引起的,而是由心血管超负荷引发的心肌细胞凋亡增强所致。此外,新生儿胸腺细胞和发育中的神经元细胞发生凋亡性细胞死亡。 Smg GDS-/-胸腺细胞易受凋亡诱导剂的影响,例如依托泊苷和紫外线照射。 Smg GDS-/-胸腺细胞通过Smg GDS cDNA的离体转导保护免受依托泊苷诱导的细胞死亡。这些表型与在Ki-Ras缺陷型小鼠中观察到的表型部分重合,表明Smg GDS参与了通过Ki-Ras的抗凋亡细胞存活信号转导。

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