PHD3-dependent hydroxylation of HCLK2 promotes the DNA damage response Full Text
The Journal of Clinical Investigation, 08/01/2012
Xie L et al. – These identification of HCLK2 as a substrate of PHD3 reveals the mechanism through which hypoxia inhibits the DDR, suggesting hydroxylation of HCLK2 is a potential therapeutic target for regulating the ATR/CHK1/p53 pathway.



