Maki Saitoh

TL;DR: In this article, the authors demonstrate that rapamycin disrupted a second mTOR complex, mTORC2, in vivo and that mTORc2 was required for the insulin-mediated suppression of hepatic gluconeogenesis.

TL;DR: It is shown that transformed human prostate epithelial cells lacking PTEN require mTORC2 to form tumors when injected into nude mice, and that deleting one copy of Rictor protects Pten heterozygous mice from prostate cancer.

TL;DR: In this article, it was shown that transformed human prostate epithelial cells lacking PTEN require mTORC2 to form tumors when injected into nude mice and that Rictor is a haploinsufficient gene and that deleting one copy protected Pten heterozygous mice from prostate cancer.

TL;DR: Compared tumors derived from two different normal human mammary epithelial cell populations, one of which was isolated using a new culture medium, found that the pre-existing differences between BPECs and HMECs strongly influence the phenotypes of their transformed derivatives.

TL;DR: It is demonstrated that rapamycin disrupted a second mTOR complex, m TORC2, in vivo and that mTORC2 was required for the insulin-mediated suppression of hepatic gluconeogenesis and was sufficient to extend life span independently from changes in glucose homeostasis.