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Chandrima Gain

Researcher at Presidency University, Kolkata

Publications -  5
Citations -  46

Chandrima Gain is an academic researcher from Presidency University, Kolkata. The author has contributed to research in topics: Autophagy & Lytic cycle. The author has an hindex of 2, co-authored 4 publications receiving 29 citations.

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Transcriptional and epigenetic modulation of autophagy promotes EBV oncoprotein EBNA3C induced B-cell survival.

TL;DR: It is demonstrated that EBNA3C elevates autophagy, which serves as a prerequisite for apoptotic inhibition and maintenance of cell growth, and offers novel-targets for potential therapeutic expansion against EBV induced B-cell lymphomas.
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Proteasomal inhibition triggers viral oncoprotein degradation via autophagy-lysosomal pathway.

TL;DR: Proteasomal inhibition reduces the colony formation ability of this important viral oncoprotein, induces apoptotic cell death and increases transcriptional activation of both latent and lytic gene expression which further promotes viral reactivation from EBV transformed B-lymphocytes.
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The role of oxidative stress in the pathogenesis of infections with coronaviruses

TL;DR: In this article , a review aims to elucidate the redox mechanisms involved in the replication of coronaviruses and associated inflammation, apoptotic pathways, autoimmunity, vascular dysfunction and tissue damage that collectively contribute to multiorgan damage.
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Identification of two novel thiophene analogues as inducers of autophagy mediated cell death in breast cancer cells.

TL;DR: In this article, the authors designed, synthesized and evaluated anti-cancer properties of a series of condensed and doubly condensed furophenanthraquinones of tanshinone derivatives on two breast cancer lines - MCF7 and MDA-MB-231.
Posted ContentDOI

Proteasomal Inhibition Triggers Viral Oncoprotein Degradation via Autophagy-Lysosomal Pathway

TL;DR: Proteasomal inhibition reduces the colony formation ability of this important viral oncoprotein, increases transcriptional activation of both latent and lytic gene expression and induces viral reactivation from EBV transformed B-lymphocytes, which offers rationale to use proteasome inhibitors as potential therapeutic strategy against multiple EBV associated B-cell lymphomas.