טוען...
Inactive Atm abrogates DSB repair in mouse cerebellum more than does Atm loss, without causing a neurological phenotype
The genome instability syndrome, ataxia-telangiectasia (A-T) is caused by null mutations in the ATM gene, that lead to complete loss or inactivation of the gene’s product, the ATM protein kinase. ATM is the primary mobilizer of the cellular response to DNA double-strand breaks (DSBs) – a broad signa...
שמור ב:
| הוצא לאור ב: | DNA Repair (Amst) |
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| Main Authors: | , , , , , , |
| פורמט: | Artigo |
| שפה: | Inglês |
| יצא לאור: |
2018
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| נושאים: | |
| גישה מקוונת: | https://ncbi.nlm.nih.gov/pmc/articles/PMC7985968/ https://ncbi.nlm.nih.gov/pubmed/30348496 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.dnarep.2018.10.001 |
| תגים: |
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