Deletion of individual Ku subunits in mice causes an NHEJ-independent phenotype potentially by altering apurinic/apyrimidinic site repair.

Deletion of individual Ku subunits in mice causes an NHEJ-independent phenotype potentially by altering apurinic/apyrimidinic site repair.

Ku70 and Ku80 form a heterodimer called Ku that forms a holoenzyme with DNA dependent-protein kinase catalytic subunit (DNA-PKCS) to repair DNA double strand breaks (DSBs) through the nonhomologous end joining (NHEJ) pathway. As expected mutating these genes in mice caused a similar DSB repair-defec...

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Bibliographic Details
Main Authors: Yong Jun Choi, Han Li, Mi Young Son, Xiao-Hong Wang, Jamie L Fornsaglio, Robert W Sobol, Moonsook Lee, Jan Vijg, Sandra Imholz, Martijn E T Dollé, Harry van Steeg, Erwin Reiling, Paul Hasty
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3900520?pdf=render

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http://europepmc.org/articles/PMC3900520?pdf=render

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