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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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Caspase-mediated cleavage of ATM during cisplatin-induced tubular cell apoptosis: inactivation of its kinase activity toward p53

TL;DR: Proteolysis of ATM by caspases may inactivate this regulatory molecule to facilitate the progression of apoptosis, suggesting a cytoprotective role of ATM in this experimental model.
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Identification of OAT1/OAT3 as Contributors to Cisplatin Toxicity

TL;DR: A previously unrecognized, OCT2‐independent pathway of cisplatin‐induced renal injury is reported that is mediated by the organic anion transporters OAT1 and OAT3, which regulates renal uptake of a mercapturic acid metabolite of cisPlatin that acts as a precursor of a potent nephrotoxin.
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OCTN1 Is a High-Affinity Carrier of Nucleoside Analogues.

TL;DR: Through transcriptomic profiling, it is determined that low expression of the ergothioneine transporter OCTN1 (SLC22A4; ETT) strongly predicts poor event-free survival and overall survival in multiple cohorts of AML patients receiving treatment with the cytidine nucleoside analogue cytarabine.
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Effects of targeted Bcl-2 expression in mitochondria or endoplasmic reticulum on renal tubular cell apoptosis.

TL;DR: The results suggest that the cytoprotective effects of Bcl-2 in different renal injury models are largely determined by its subcellular localizations.
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Hypoxia-induced upregulation of BMX kinase mediates therapeutic resistance in acute myeloid leukemia

TL;DR: The results demonstrate that hypoxia-dependent upregulation of BMX contributes to therapeutic resistance through a compensatory prosurvival signaling mechanism and reveal the role of off-target drug effects on tumor microenvironment and development of acquired drug resistance.