ATR phosphorylates SMARCAL1 to prevent replication fork collapse

The DNA damage response kinase ataxia telangiectasia and Rad3-related (ATR) coordinates much of the cellular response to replication stress. The exact mechanisms by which ATR regulates DNA synthesis in conditions of replication stress are largely unknown, but this activity is critical for the viabil...

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Vydáno v:	Genes & development Ročník 27; číslo 14; s. 1610
Hlavní autoři:	Couch, Frank B, Bansbach, Carol E, Driscoll, Robert, Luzwick, Jessica W, Glick, Gloria G, Bétous, Rémy, Carroll, Clinton M, Jung, Sung Yun, Qin, Jun, Cimprich, Karlene A, Cortez, David
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States 15.07.2013
Témata:	Animals Ataxia Telangiectasia Mutated Proteins Cell Cycle Proteins - metabolism Cell Line, Tumor Cell Survival - drug effects DNA Damage - drug effects DNA Helicases - genetics DNA Helicases - metabolism DNA Replication - drug effects DNA Replication - physiology DNA, Single-Stranded - genetics Enzyme Activation Humans Phosphorylation - drug effects Protein Binding Protein Kinase Inhibitors - pharmacology Protein-Serine-Threonine Kinases - metabolism Xenopus SMARCAL1 DNA replication DNA damage response HARP cell cycle checkpoint ATR
ISSN:	1549-5477, 1549-5477
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