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Amanda K. Ashley
Researcher at New Mexico State University
Publications - 24
Citations - 776
Amanda K. Ashley is an academic researcher from New Mexico State University. The author has contributed to research in topics: DNA repair & DNA. The author has an hindex of 13, co-authored 23 publications receiving 670 citations. Previous affiliations of Amanda K. Ashley include Colorado State University & Mayo Clinic.
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Journal ArticleDOI
Distinct roles for DNA-PK, ATM and ATR in RPA phosphorylation and checkpoint activation in response to replication stress
Shengqin Liu,Stephen O. Opiyo,Karoline C. Manthey,Jason G. Glanzer,Amanda K. Ashley,Courtney Amerin,Kyle Troksa,Meena Shrivastav,Jac A. Nickoloff,Jac A. Nickoloff,Greg G. Oakley +10 more
TL;DR: It is shown that DNA- PKcs mutant cells fail to arrest replication following stress, and mutations in RPA32 phosphorylation sites targeted by DNA-PKcs increase the proportion of cells in mitosis, impair ATR signaling to Chk1 and confer a G2/M arrest defect.
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More forks on the road to replication stress recovery
TL;DR: It is imperative to gain a better understanding of replication stress response proteins and pathways to improve cancer therapy, as most cancer therapeutic strategies create DNA replication stress.
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DNA-PK phosphorylation of RPA32 Ser4/Ser8 regulates replication stress checkpoint activation, fork restart, homologous recombination and mitotic catastrophe.
Amanda K. Ashley,Meena Shrivastav,Jingyi Nie,Courtney Amerin,Kyle Troksa,Jason G. Glanzer,Shengqin Liu,Stephen O. Opiyo,Diana D. Dimitrova,Phuong Le,Brock J. Sishc,Susan M. Bailey,Gregory G. Oakley,Jac A. Nickoloff,Jac A. Nickoloff +14 more
TL;DR: It is shown that DNA-PK and ATR signaling through RPA32 plays a critical role in promoting genome stability and cell survival in response to replication stress, and that hyper-recombination in these mutants is ATM-dependent, but the other defects are ATM-independent.
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Cellular and Phenotypic Characterization of Canine Osteosarcoma Cell Lines
TL;DR: Of particular interest, the robust growth of a subcutaneous tumor and rapid pulmonary metastasis of the Abrams cell line in an immunocompromised mouse shows incredible potential for the future use of Abrams as a canine OSA model.
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Progestin-mediated activation of MAPK and AKT in nuclear progesterone receptor negative breast epithelial cells: The role of membrane progesterone receptors.
TL;DR: The results add to the understanding that various progestins have on breast epithelial cells and underscores the importance of considering both membrane bound receptors and progestin type in breast cancer development.