In conclusion, PCAF regulates the balance between cell-cycle arrest and apoptosis in hypoxia by modulating the activity and protein stability of both p53 and HIF-1alpha.
Cardiac angiogenesis played an important role in the maintenance of cardiac function as well as the development of cardiac hypertrophy induced by pressure-overload, and upregulated p53 induced the transition from cardiac hypertrophy to heart failure through the suppression of hypoxia inducible factor-1(HIF-1), which regulates angiogenesis in the hypertrophied heart.
Interestingly, however, DNA damage combined with hypoxia modulated both the intensity of the p53 response and the composition of downstream target genes.
However, we found that Fas/CD95 was significantly induced in response to hypoxia in a p53-dependent manner, along with several novel p53 target genes including ANXA1, DDIT3/GADD153 (CHOP), SEL1L and SMURF1.