DNA lesions and DNA damage response: even long lasting relationships need a "break".
The elucidation of the spatiotemporal map of the DNA damage response (DDR) has been critical to our understanding of how cells are protected against insults to genomic integrity. Recruitment and transient immobilization at DNA breaks is a typical characteristic of many DDR proteins. Here, I discuss evidence that stable association of DDR proteins with chromatin is sufficient to activate the DDR even in the absence of damage. These observations critically support the notion that nuclear repair compartments play a primary role in triggering and amplifying DDR.
Soutoglou
Evi
E
National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. evisou@igbmc.fr
D000818:Animals; D064007:Ataxia Telangiectasia Mutated Proteins; D018797:Cell Cycle Proteins / Q000378:metabolism; D004249:DNA Damage; D004260:DNA Repair; D004268:DNA-Binding Proteins / Q000378:metabolism; D006801:Humans; D008954:Models, Biological; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D025521:Tumor Suppressor Proteins / Q000378:metabolism
D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; D025521:Tumor Suppressor Proteins; C576324:ATM protein, human; D064007:Ataxia Telangiectasia Mutated Proteins; D017346:Protein Serine-Threonine Kinases