Late after infection, several checkpoint proteins, including ataxia-telangiectasia mutated and Chk2, are mislocalized to a cytoplasmic virus assembly zone, where they are colocalized with virion structural proteins.
However, this activation does not propagate through the pathway it is blocked at the level of the effector kinase, checkpoint kinase 2 (Chk2). Here we show that the ataxia-telangiectasia mutated checkpoint pathway, which responds to double-strand breaks in DNA, is activated in response to human cytomegalovirus DNA replication. Several viruses are known to activate or modulate this cellular response.
The DNA damage checkpoint pathway responds to DNA damage and induces a cell cycle arrest to allow time for DNA repair.
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