The Werner syndrome protein at the crossroads of DNA repair and apoptosis
作者： Lucio Comai , Baomin Li
DOI: 10.1016/J.MAD.2004.06.004
关键词: Nuclear protein 、 Genetics 、 Helicase 、 DNA 、 Premature aging 、 Biology 、 Senescence 、 Gene 、 DNA repair 、 Werner syndrome
摘要: Werner syndrome (WS) is a premature aging disease characterized by genetic instability. WS caused mutations in gene encoding for 160 kDa nuclear protein, the protein (WRN), which has exonuclease and helicase activities. The mechanism whereby WRN controls genome stability life span not known. Over last few years, become focus of intense investigation growing number scientists. studies carried out many laboratories have provided wealth new information about functional properties its cellular partners. This review focuses on recent findings that demonstrate interaction between two factors bind to DNA breaks, Ku poly(ADP-ribose) polymerase 1, discuss how these interactions can influence fundamental processes such as repair, apoptosis possibly regulate cell senescence organismal aging.
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