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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Veröffentlicht in:	PloS one 2014-01, Vol.9 (1), p.e86358
Hauptverfasser:	Choi, Yong Jun, Li, Han, Son, Mi Young, Wang, Xiao-Hong, Fornsaglio, Jamie L, Sobol, Robert W, Lee, Moonsook, Vijg, Jan, Imholz, Sandra, Dollé, Martijn E T, van Steeg, Harry, Reiling, Erwin, Hasty, Paul
Format:	Artikel
Sprache:	eng
Schlagworte:	Addition polymerization Aging Animals Antigens, Nuclear - genetics AP endonuclease Apurinic Acid - genetics Base excision repair Biology Brain Cancer Catalysis Cell death Clonal deletion Defects Deoxyribonucleic acid DNA DNA damage DNA End-Joining Repair DNA polymerase DNA repair DNA-(Apurinic or Apyrimidinic Site) Lyase - antagonists & inhibitors DNA-Activated Protein Kinase - deficiency DNA-Activated Protein Kinase - genetics DNA-Binding Proteins - deficiency DNA-Binding Proteins - genetics DNA-directed DNA polymerase Endonuclease Enzymes Epistasis Epistasis, Genetic Female Gene Deletion Genetic aspects Genomes Genotype & phenotype House mouse Indoles - pharmacology Kinases Ku Autoantigen Lesions Life span Longevity Male Medical research Medicine Mice Mice, Inbred C57BL Mice, Knockout Mutation Non-homologous end joining Nuclear Proteins - deficiency Nuclear Proteins - genetics p53 Protein Pharmacology Phenotype Point Mutation Protein kinase Protein kinase C Protein kinases Protein Subunits - deficiency Protein Subunits - genetics Proteins Public health Radiation Tolerance Reagents Repair Rodents Science Senescence Tumor proteins Tumor Suppressor Protein p53 - metabolism
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