Ras-related C3 botulinum toxin substrate 1 (RAC1) regulates glucose-stimulated insulin secretion via modulation of F-actin

@inproceedings{Asahara2013RasrelatedCB,
  title={Ras-related C3 botulinum toxin substrate 1 (RAC1) regulates glucose-stimulated insulin secretion via modulation of F-actin},
  author={Shun-ichiro Asahara and Yuki Shibutani and Kyoko Teruyama and H. Inoue and Yukina Kawada and Hiroaki Etoh and Takeru Matsuda and Maki Kimura-Koyanagi and Nobuhiro Hashimoto and M. Sakahara and Wakako Fujimoto and Hachidai Takahashi and Sunao Ueda and Tetsuya Hosooka and Takaya Satoh and Michihiro Matsumoto and Atsu Aiba and Masato Kasuga and Yoshiaki Kido},
  booktitle={Diabetologia},
  year={2013}
}
The small G-protein ras-related C3 botulinum toxin substrate 1 (RAC1) plays various roles in mammalian cells, such as in the regulation of cytoskeletal organisation, cell adhesion, migration and morphological changes. The present study examines the effects of RAC1 ablation on pancreatic beta cell function. Isolated islets from pancreatic beta cell-specific Rac1-knockout (betaRac1 −/−) mice and RAC1 knockdown INS-1 insulinoma cells treated with small interfering RNA were used to investigate… CONTINUE READING