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Collaboration of Brca1 and Chk2 in tumorigenesis
Disruption of Brca1 results in cellular demise or tumorigenesis depending on cellular context. Inactivation of p53 contributes to Brca1-associated tumor susceptibility. However the activation of p53-dependent checkpoint/apoptotic signaling in the absence of Brca1 is poorly understood. Here, we show...
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主要な著者: | , , , , , , , , , , , , , |
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フォーマット: | Artigo |
言語: | Inglês |
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Cold Spring Harbor Laboratory Press
2004
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オンライン・アクセス: | https://ncbi.nlm.nih.gov/pmc/articles/PMC415639/ https://ncbi.nlm.nih.gov/pubmed/15131084 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1101/gad.1192704 |
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