Nivedita Chatterjee

Dr. Nivedita Chatterjee

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Research Focus & Metrics

Academic Career Length

17Years (2010-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 March 2014 in Molecular and Cellular Neuroscience
Verified
Journal Article
Closed access
GKGopinath Krishnan
Gopinath Krishnan
NCNivedita Chatterjee
Nivedita Chatterjee

1 January 2015 in Neuroscience
Verified
Journal Article
Closed access
GKG. Krishnan
G. Krishnan
NCNivedita Chatterjee
Nivedita Chatterjee

28 January 2011 in Journal of Neuroimmune Pharmacology
Verified
Journal Article
Closed access
PDF file
NCNivedita Chatterjee
Nivedita Chatterjee
SCShannon Callen
Shannon Callen
GSGail M. Seigel
Gail M. Seigel
SBShilpa Buch
Shilpa Buch

10 August 2022 in Ocular Immunology and Inflammation
Verified
Journal Article
Closed access
DDDurairaj Duraikkannu
Durairaj Duraikkannu
AAAshraf Banu Akbar
Ashraf Banu Akbar
SSSridharan Sudharshan
Sridharan Sudharshan
SPSelvamuthu Poongulali
Selvamuthu Poongulali
NKNagalingeswaran Kumarasamy
Nagalingeswaran Kumarasamy
NCNivedita Chatterjee
Nivedita Chatterjee
Notwithstanding well-established clinical features of Immune Recovery Uveitis (IRU), specific diagnostic tools to identify at-risk patients are lacking. Identification of biomarkers for IRU predict...

3 June 2024 in Viruses
Verified
Journal Article
Open access
UDUma Maheswari Deshetty
Uma Maheswari Deshetty
NCNivedita Chatterjee
Nivedita Chatterjee
SBShilpa Buch
Shilpa Buch
PPPalsamy Periyasamy
Palsamy Periyasamy
Antiretroviral treatments have notably extended the lives of individuals with HIV and reduced the occurrence of comorbidities, including ocular manifestations. The involvement of endoplasmic reticulum (ER) stress in HIV-1 pathogenesis raises questions about its correlation with cellular senescence or its role in initiating senescent traits. This study investigated how ER stress and dysregulated autophagy impact cellular senescence triggered by HIV-1 Tat in the MIO-M1 cell line (human Müller glial cells). Cells exposed to HIV-1 Tat exhibited increased vimentin expression combined with markers of ER stress (BiP, p-eIF2α), autophagy (LC3, Beclin-1, p62), and the senescence marker p21 compared to control cells. Western blotting and staining techniques like SA-β-gal were employed to examine these markers. Additionally, treatments with ER stress inhibitor 4-PBA before HIV-1 Tat exposure led to a decreased expression of ER stress, senescence, and autophagy markers. Conversely, pre-treatment with the autophagy inhibitor 3-MA resulted in reduced autophagy and senescence markers but did not alter ER stress markers compared to control cells. The findings suggest a link between ER stress, dysregulated autophagy, and the initiation of a senescence phenotype in MIO-M1 cells induced by HIV-1 Tat exposure.