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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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| 主要な著者: | , , , , , , , , , , , , |
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| フォーマット: | Artigo |
| 言語: | Inglês |
| 出版事項: |
Public Library of Science (PLoS)
2014-01-01
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| シリーズ: | PLoS ONE |
| オンライン･アクセス: | http://europepmc.org/articles/PMC3900520?pdf=render |
| タグ: |
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