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Navjotsingh Pabla
Researcher at Ohio State University
Publications - 44
Citations - 3621
Navjotsingh Pabla is an academic researcher from Ohio State University. The author has contributed to research in topics: Cisplatin & Acute kidney injury. The author has an hindex of 21, co-authored 33 publications receiving 3052 citations. Previous affiliations of Navjotsingh Pabla include Charlie Norwood VA Medical Center & Georgia Regents University.
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Journal ArticleDOI
Cisplatin nephrotoxicity: Mechanisms and renoprotective strategies
Navjotsingh Pabla,Zheng Dong +1 more
TL;DR: Examination of tumor-bearing animals and identification of novel renoprotective strategies that do not diminish the anticancer efficacy of cisplatin are essential to the development of clinically applicable interventions.
Journal Article
ATR-Chk2 signaling in p53 activation and DNA damage response during cisplatin-induced apoptosis (Journal of Biological Chemistry (2008) 283, (6572-6583))
TL;DR: It is shown that ATR is specifically activated during cisplatin treatment and co-localizes with H2AX, forming nuclear foci at the site of DNA damage, suggesting an important role for the DNA damage response mediated by ATR-Chk2 in p53 activation and renal cell apoptosis during cisPlatin nephrotoxicity.
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ATR-Chk2 signaling in p53 activation and DNA damage response during cisplatin-induced apoptosis
TL;DR: In this article, the authors demonstrate an early DNA damage response during cisplatin treatment of renal cells and tissues, and demonstrate a critical role for ATR, but not ATM (ataxia telangiectasia mutated) or DNA-PK (DNA-dependent protein kinase), in the activation and apoptosis of kidney cells.
Journal ArticleDOI
The copper transporter Ctr1 contributes to cisplatin uptake by renal tubular cells during cisplatin nephrotoxicity.
TL;DR: First evidence for a role of Ctr1 in cisplatin uptake and nephrotoxicity is demonstrated, mainly expressed in both proximal and distal tubular cells in mouse kidneys.
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Checkpoint kinase 1 in DNA damage response and cell cycle regulation
TL;DR: Originally identified as a mediator of DNA damage response (DDR), checkpoint kinase 1 (Chk1) has a broader role in checkpoint activation in DDR and normal cell cycle regulation and may be an effective therapeutic target in diseases such as cancer.