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Brian M. Cartwright
Researcher at East Tennessee State University
Publications - 12
Citations - 261
Brian M. Cartwright is an academic researcher from East Tennessee State University. The author has contributed to research in topics: DNA damage & Phosphorylation. The author has an hindex of 5, co-authored 11 publications receiving 212 citations.
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Journal ArticleDOI
DNA-PK, ATM and ATR collaboratively regulate p53-RPA interaction to facilitate homologous recombination DNA repair.
Moises A. Serrano,Zhengke Li,Mohan Dangeti,Phillip R. Musich,Steve M. Patrick,Marina Roginskaya,Brian M. Cartwright,Yue Zou +7 more
TL;DR: The results reveal a mechanism for the crosstalk between HR repair and NHEJ through the co-regulation of p53–RPA interaction by DNA-PK, ATM and ATR.
Journal ArticleDOI
ATR Plays a Direct Antiapoptotic Role at Mitochondria, which Is Regulated by Prolyl Isomerase Pin1
Benjamin Hilton,Zhengke Li,Phillip R. Musich,Hui Wang,Brian M. Cartwright,Moises A. Serrano,Xiao Zhen Zhou,Kun Ping Lu,Yue Zou +8 more
TL;DR: It is reported that ATR has an antiapoptotic activity at mitochondria in response to UV damage, and this activity is independent of its hallmark checkpoint/kinase activity and partner ATRIP.
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Progerin sequestration of PCNA promotes replication fork collapse and mislocalization of XPA in laminopathy-related progeroid syndromes.
Benjamin Hilton,Ji Liu,Brian M. Cartwright,Yiyong Liu,Maya Breitman,Youjie Wang,Rowdy Jones,Hui Tang,Antonio E. Rusiñol,Phillip R. Musich,Yue Zou +10 more
TL;DR: It is demonstrated that progerin‐induced apoptosis could be rescued by XPA, suggesting that XPA‐replication fork binding may prevent apoptosis in HGPS cells, and sequestration of PCNA promotes replication fork collapse and mislocalization of XPA in laminopathy‐related progeroid syndromes.
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UV-Induced Nuclear Import of XPA Is Mediated by Importin-α4 in An ATR-Dependent Manner
TL;DR: Results suggest that upon DNA damage transport adaptor importin-α4 imports XPA into the nucleus in an ATR-dependent manner, while XAB1 has no role in this process, revealing a potential new therapeutic target for the sensitization of cancer cells to chemotherapy.
Journal ArticleDOI
Insulin resistance and muscle insulin receptor substrate-1 serine hyperphosphorylation
Charles A. Stuart,Mary E. A. Howell,Brian M. Cartwright,Melanie P. McCurry,M. Lee,Michael W. Ramsey,Michael H. Stone +6 more
TL;DR: Excess fasting phosphorylation of muscle IRS‐1 at Ser636 may be a major cause of the insulin resistance seen in obesity and might prevent improvement in insulin responsiveness when exercise training is not accompanied by weight loss.