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Nihar Ranjan Jana

Researcher at Indian Institute of Technology Kharagpur

Publications -  100
Citations -  11041

Nihar Ranjan Jana is an academic researcher from Indian Institute of Technology Kharagpur. The author has contributed to research in topics: Proteasome & Huntingtin. The author has an hindex of 37, co-authored 96 publications receiving 9985 citations. Previous affiliations of Nihar Ranjan Jana include RIKEN Brain Science Institute & National Institute for Environmental Studies.

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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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Trehalose alleviates polyglutamine-mediated pathology in a mouse model of Huntington disease.

Motomasa Tanaka, +8 more
- 18 Jan 2004 - 
TL;DR: Oral administration of trehalose, the most effective of these disaccharides, decreased polyglutamine aggregates in cerebrum and liver, improved motor dysfunction and extended lifespan in a transgenic mouse model of Huntington disease, making trehalOSE promising as a therapeutic drug or lead compound for the treatment of polyglUTamine diseases.
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Altered proteasomal function due to the expression of polyglutamine-expanded truncated N-terminal huntingtin induces apoptosis by caspase activation through mitochondrial cytochrome c release

Nihar Ranjan Jana, +3 more
- 01 May 2001 - 
TL;DR: The impaired proteasomal function plays an important role in polyglutamine protein-induced cell death and is associated with disrupted mitochondrial membrane potential, released cytochrome c from mitochondria into the cytosol and activated caspase-9- and caspases-3-like proteases.
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Polyglutamine length-dependent interaction of Hsp40 and Hsp70 family chaperones with truncated N-terminal huntingtin: their role in suppression of aggregation and cellular toxicity

Nihar Ranjan Jana, +3 more
- 12 Aug 2000 - 
TL;DR: Overexpression of Hdj-1 and Hsc70 is also able to protect cell death caused by polyglutamine-expanded tNhtt and their combination proved to be most effective and strongly suggests that the chaperone interaction and their redistribution to the aggregates are two completely different phenomena of the cellular unfolded protein response.
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Co-chaperone CHIP Associates with Expanded Polyglutamine Protein and Promotes Their Degradation by Proteasomes

Nihar Ranjan Jana, +6 more
- 25 Mar 2005 - 
TL;DR: It is demonstrated that CHIP (C terminus of Hsp70-interacting protein) co-immunoprecipitates with the polyglutamine-expanded huntingtin or ataxin-3 and associates with their aggregates and suppressive effect is more prominent when CHIP is overexpressed along with Hsc70.