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ATMIN is required for the ATM-mediated signaling and recruitment of 53BP1 to DNA damage sites upon replication stress
Unresolved replication intermediates can block the progression of replication forks and become converted into DNA lesions, hence exacerbating genomic instability. The p53-binding protein 1 (53BP1) forms nuclear bodies at sites of unrepaired DNA lesions to shield these regions against erosion, in a m...
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| Pubblicato in: | DNA Repair (Amst) |
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| Autori principali: | , , , , , , |
| Natura: | Artigo |
| Lingua: | Inglês |
| Pubblicazione: |
Elsevier
2014
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| Soggetti: | |
| Accesso online: | https://ncbi.nlm.nih.gov/pmc/articles/PMC4251980/ https://ncbi.nlm.nih.gov/pubmed/25262557 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.dnarep.2014.09.001 |
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