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PMID |
Sentence |
1 |
16906222
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However, a report published in a recent issue of the International Journal of Biological Sciences revealed that PARP-1 inhibitors, although able to kill naïve BRCA1 mutant cells with high specificity both in vitro and in vivo, exhibit minimal specificity in inhibiting the growth of mouse mammary tumor cells irrespective of their BRCA1 status in allograft nude mice.
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2 |
16906222
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Non-specific inhibition in human BRCA1+/+, BRCA1+/-, and BRCA1-/- breast cancer cells by PARP-1 inhibitors was also observed.
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3 |
17620310
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Breast cancer-associated mutations affecting the highly-conserved C-terminal BRCT domains of the tumor suppressor gene breast cancer susceptibility gene 1 (BRCA1) fully disrupt the ability of BRCA1 to interact with acetyl coenzyme A carboxylase alpha (ACCA), the rate-limiting enzyme catalyzing de novo fatty acid biogenesis.
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4 |
17620310
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Specifically, BRCA1 interacts solely with the phosphorylated (inactive) form of ACCA (P-ACCA), and the formation of the BRCA1/P-ACCA complex interferes with ACCA activity by preventing P-ACCA dephosphorylation.
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5 |
17620310
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Alternatively, new forthcoming ACCA inhibitors may be relevant in the management of BRCA1-dependent breast cancer susceptibility and development.
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6 |
15485917
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After DNA damage, BRCA1 is phosphorylated by CHK2 at serine 988, followed by a change in its intracellular location.
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7 |
15485917
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We demonstrated that the Brca1(S971A/S971A) cells displayed reduced ability to activate the G(2)/M cell cycle checkpoint upon gamma-irradiation and to stabilize p53 following N-methyl-N'-nitro-N-nitrosoguanidine treatment.
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8 |
16675955
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Analysis of Brca1(delta11/delta11)Chk2-/- mice revealed that p53-dependent apoptosis and growth defect caused by Brca1 deficiency are significantly attenuated in rapidly proliferating organs.
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