Kathrin Gottlob

TL;DR: The disruption of the most ubiquitously expressed member of the akt family of genes, akt1, in the mouse is reported, resulting in viable but smaller mice and mice that are more susceptible to apoptosis induced by TNF, anti-Fas, UV irradiation, and serum withdrawal.

TL;DR: It is proposed that Akt increases coupling of glucose metabolism to oxidative phosphorylation and regulates PT pore opening via the promotion of hexokinase-VDAC interaction at the outer mitochondrial membrane.

TL;DR: Genetic evidence is provided thatAkt is required to maintain hexokinase association with mitochondria and that changes in outer mitochondrial membrane permeability leading to apoptosis can occur in the absence of Bax and Bak and that Akt inhibits these changes through maintenance of hexokin enzyme association with mitochondrial.

TL;DR: In this paper, the authors investigated the anti-apoptotic role of hexokinases (HKs) in the protection of epithelial cells from acute oxidant-induced cell death.

TL;DR: It is shown for the first time that, in addition to mutations in complementary antiapoptotic genes, c-Myc itself can acquire mutations that potentiate neoplastic transformation by affecting apoptosis independently of cell cycle progression.