Mitochondrial H2O2 Regulates the Angiogenic Phenotype via PTEN Oxidation

Tumours and tremors: how PTEN regulation underlies both

“…This type of PTEN inactivation is seen in cell cultures following growth factor-induced peroxide production, suggesting that redox inactivation of PTEN is a physiologic response to mitogen stimulation (Kwon et al, 2004). Consistent with this hypothesis, increases in hydrogen peroxide specifically induced by mitochondrial dysfunction lead to the oxidation and inactivation of PTEN and increased PI3 0 K signalling (Connor et al, 2005). The ability of oxidised PTEN to regain its tumour suppressive activity depends on the capacity of thioredoxin to reduce the inactive form, and a total loss of PTEN function can occur if the redox status of the cell is abnormal Kwon et al, 2004).…”

When a theory of aging ages badly

“…The mitochondria from the transgenic mice seem resistant to oxidative stress but aconitase activity in the absence of an exogenous treatment is not higher than controls thus suggesting that intra-mitochondrial oxidative status is unaffected by MCAT expression [31]. Moreover, knowing that catalase is a major hydrogen peroxide scavenger and that this particular ROS is now considered as an important mediator in mitochondrial signal transduction [35][36][37] it is difficult to exclude the possibility that the longevity phenotype did not directly result from reduced mitochondrial oxidative stress.…”

PTEN: a default gate-keeping tumor suppressor with a versatile tail

“…Indeed, PTEN has been reported to be modified in multiple ways including phosphorylation [31][32][33][34], oxidation [35][36][37] and the recently reported nitrosylation [38]. Progress along these lines has been limited although it is clear that all these modifications exert negative regulatory effects on PTEN function.…”