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Gopal Chakrabarti

Researcher at University of Calcutta

Publications -  63
Citations -  8155

Gopal Chakrabarti is an academic researcher from University of Calcutta. The author has contributed to research in topics: Microtubule & Tubulin. The author has an hindex of 23, co-authored 63 publications receiving 6541 citations. Previous affiliations of Gopal Chakrabarti include University of Kansas & Shiv Nadar University.

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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.
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
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miR-17-5p downregulation contributes to paclitaxel resistance of lung cancer cells through altering beclin1 expression.

TL;DR: It is demonstrated that miR-17-5p directly binds to the 3′-UTR of beclin 1 gene, one of the most important autophagy modulator, and indicated that paclitaxel resistance of lung cancer is associated with downregulation of miR -17- 5p expression which might cause upregulation of BECN1 expression.
Journal ArticleDOI

Unprecedented inhibition of tubulin polymerization directed by gold nanoparticles inducing cell cycle arrest and apoptosis

TL;DR: This first observation of nanoparticles-induced protein's conformational change-based aggregation of the tubulin-MT system is of high importance, and would be useful in the understanding of cancer therapeutics and safety of nanomaterials.
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MiR-16 targets Bcl-2 in paclitaxel-resistant lung cancer cells and overexpression of miR-16 along with miR-17 causes unprecedented sensitivity by simultaneously modulating autophagy and apoptosis.

TL;DR: It was demonstrated that anti-apoptotic protein Bcl-2 was directly targeted miR-16 in paclitaxel resistant lung cancer cells and the combined overexpression of mi R-16 and miR -17 and subsequent pac litaxel treatment greatly sensitized paclitAXel resistant Lung cancer cells to paclitaxeel by inducing apoptosis via caspase-3 mediated pathway.