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Subbiah Pugazhenthi

Researcher at Veterans Health Administration

Publications -  81
Citations -  9552

Subbiah Pugazhenthi is an academic researcher from Veterans Health Administration. The author has contributed to research in topics: CREB & Insulin. The author has an hindex of 34, co-authored 79 publications receiving 8659 citations. Previous affiliations of Subbiah Pugazhenthi include Anschutz Medical Campus & United States Department of Veterans Affairs.

Papers
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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Akt/protein kinase B up-regulates Bcl-2 expression through cAMP-response element-binding protein.

TL;DR: Data indicate that regulation of Bcl-2 expression by IGF-I involves a signaling cascade mediated by PI 3-kinase/PDK1/Akt/CREB, and the observation that enhanced CREB activity by Akt signaling leads to increased B cl-2 promoter activity and cell survival.
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Common neurodegenerative pathways in obesity, diabetes, and Alzheimer's disease ☆

TL;DR: Molecular mechanisms that link obesity, diabetes and AD, including oxidative stress, mitochondrial dysfunction, and inflammation that are observed in these disorders are discussed.
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Downregulation of CREB expression in Alzheimer's brain and in Aβ-treated rat hippocampal neurons.

TL;DR: The findings suggest that chronic downregulation of CREB-mediated transcription results in decrease ofCREB content in the hippocampal neurons of AD brain which may contribute to exacerbation of disease progression.
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Oxidative Stress in Type 1 Diabetes

TL;DR: It is demonstrated that treatment of prediabetic NOD mice for 2 weeks with a metalloporphyrin superoxide dismutase (SOD) mimetic results in marked reduction of oxidative stress in islets and vascular tissue and a reversal of macrophage defects.