Published in Gene Therapy Weekly, July 6th, 2006
Study 1: A study from the United States has reported that priming phosphorylation of Chk2 by polo-like kinase 3 (Plk3) mediates its full activation by ataxia-telangiectasia mutated (ATM) and a downstream checkpoint in response to DNA damage.
"The tumor suppressor gene Chk2 encodes a Ser/Thr kinase that signals DNA damage to cell cycle checkpoints. In response to ionizing radiation, Chk2 is phosphorylated on Thr 68 (T68) by ATM protein leading to its activation," wrote E.M. Bahassi and colleagues, University of Cincinnati.
"We have previously shown that...
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