J
Jana Mahadevan
Researcher at Washington University in St. Louis
Publications - 16
Citations - 939
Jana Mahadevan is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Wolfram syndrome & Endoplasmic reticulum. The author has an hindex of 11, co-authored 16 publications receiving 728 citations. Previous affiliations of Jana Mahadevan include Daiichi Sankyo & Pacific Northwest Diabetes Research Institute.
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Journal ArticleDOI
Calcium Efflux From the Endoplasmic Reticulum Leads to β-Cell Death
TL;DR: The results reveal a critical role of ER calcium depletion in β-cell death and indicate that identification of pathways and chemical compounds restoring ER calcium levels will lead to novel therapeutic modalities and pharmacological interventions for type 1 and type 2 diabetes and other ER-related diseases including Wolfram syndrome.
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Poly-dipeptides encoded by the C9ORF72 repeats block global protein translation
Kohsuke Kanekura,Takuya Yagi,Alexander J. Cammack,Jana Mahadevan,Masahiko Kuroda,Matthew B. Harms,Timothy M. Miller,Fumihiko Urano +7 more
TL;DR: It is demonstrated that impaired protein translation mediated by poly-PR and poly-GR peptides plays a role in neurotoxicity and revealed that the pathways altered by the poly-dipeptides-mRNA complexes are potential therapeutic targets for treatment of C9orf72 FTD/ALS.
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A calcium-dependent protease as a potential therapeutic target for Wolfram syndrome.
Simin Lu,Kohsuke Kanekura,Takashi Hara,Jana Mahadevan,Larry D. Spears,Christine M. Oslowski,Rita Martinez,Mayu Yamazaki-Inoue,Masashi Toyoda,Amber M. Neilson,Patrick Blanner,Cris M. Brown,Clay F. Semenkovich,Bess A. Marshall,Tamara Hershey,Akihiro Umezawa,Peter A. Greer,Fumihiko Urano +17 more
TL;DR: It is reported that the pathway leading to calpain activation offers potential drug targets for Wolfram syndrome and substrates for calpain might serve as biomarkers for this syndrome, and that dantrolene can prevent cell death in neural progenitor cells derived fromWolfram syndrome iPS cells.
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Intermittent fasting preserves beta-cell mass in obesity-induced diabetes via the autophagy-lysosome pathway
Haiyan Liu,Ali Javaheri,Rebecca J. Godar,John T. Murphy,Xiucui Ma,Nidhi Rohatgi,Jana Mahadevan,Krzysztof L. Hyrc,Paul Saftig,Connie A. Marshall,Michael L. McDaniel,Maria S. Remedi,Babak Razani,Fumihiko Urano,Abhinav Diwan +14 more
TL;DR: Data show that despite continued high-fat intake, intermittent fasting restores autophagic flux in islets and improves glucose tolerance by enhancing glucose-stimulated insulin secretion, beta cell survival, and nuclear expression of NEUROG3, a marker of pancreatic regeneration.
Journal ArticleDOI
Autosomal Dominant Diabetes Arising From a Wolfram Syndrome 1 Mutation
Lori L. Bonnycastle,Peter S. Chines,Takashi Hara,Jeroen R. Huyghe,Amy J. Swift,Pirkko Heikinheimo,Jana Mahadevan,Sirkku Peltonen,Hanna Huopio,Pirjo Nuutila,Pirjo Nuutila,Narisu Narisu,Rachel L. Goldfeder,Michael L. Stitzel,Simin Lu,Michael Boehnke,Fumihiko Urano,Francis S. Collins,Markku Laakso +18 more
TL;DR: A novel nonsynonymous variant (p.Trp314Arg) in the Wolfram syndrome 1 (WFS1) gene is uncovered that segregates completely with the diabetic phenotype and represents the first compelling report of a mutation in WFS1 associated with dominantly inherited nonsyndromic adult-onset diabetes.