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The guanine nucleotide exchange factor FLJ00068 activates Rac1 in adipocyte insulin signaling
FEBS Letters ( IF 3.5 ) Pub Date : 2020-10-09 , DOI: 10.1002/1873-3468.13939
Nobuyuki Takenaka 1 , Mika Nakao 1 , Kiko Hasegawa 1 , Man Piu Chan 1 , Takaya Satoh 1
Affiliation  

Insulin stimulates glucose uptake via the translocation of the glucose transporter GLUT4 to the plasma membrane in adipocytes. Several lines of evidence suggest that the small GTPase Rac1 plays an important role in insulin‐stimulated glucose uptake in skeletal muscle and adipocytes. The purpose of this study is to investigate the mechanisms whereby Rac1 is regulated in adipocyte insulin signaling. Here, we show that knockdown of the guanine nucleotide exchange factor FLJ00068 inhibits Rac1 activation and GLUT4 translocation by insulin and a constitutively activated form of the protein kinase Akt2. Furthermore, constitutively activated FLJ00068 induced Rac1 activation and Rac1‐dependent GLUT4 translocation. Collectively, these results suggest the involvement of FLJ00068 downstream of Akt2 in insulin‐stimulated glucose uptake signaling in adipocytes.

中文翻译:

鸟嘌呤核苷酸交换因子 FLJ00068 激活脂肪细胞胰岛素信号中的 Rac1

胰岛素通过葡萄糖转运蛋白 GLUT4 易位到脂肪细胞的质膜来刺激葡萄糖摄取。多项证据表明,小 GTPase Rac1 在骨骼肌和脂肪细胞中胰岛素刺激的葡萄糖摄取中起重要作用。本研究的目的是研究 Rac1 在脂肪细胞胰岛素信号传导中受到调节的机制。在这里,我们展示了鸟嘌呤核苷酸交换因子 FLJ00068 的组合式抑制了胰岛素和蛋白激酶 Akt2 的组成型激活形式的 Rac1 激活和 GLUT4 易位。此外,组成型激活的 FLJ00068 诱导 Rac1 激活和 Rac1 依赖性 GLUT4 易位。总的来说,这些结果表明 Akt2 下游的 FLJ00068 参与脂肪细胞中胰岛素刺激的葡萄糖摄取信号。
更新日期:2020-10-09
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