Saurabh Chattopadhyay

ORCID: 0000-0002-2930-1523
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About
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Research Areas
  • interferon and immune responses
  • Immune Response and Inflammation
  • Viral Infections and Vectors
  • Plant tissue culture and regeneration
  • Cytokine Signaling Pathways and Interactions
  • NF-κB Signaling Pathways
  • RNA regulation and disease
  • Influenza Virus Research Studies
  • Restraint-Related Deaths
  • Plant-derived Lignans Synthesis and Bioactivity
  • 14-3-3 protein interactions
  • Autopsy Techniques and Outcomes
  • Viral Infections and Outbreaks Research
  • Mosquito-borne diseases and control
  • Animal Virus Infections Studies
  • Traumatic Ocular and Foreign Body Injuries
  • Inflammasome and immune disorders
  • SARS-CoV-2 detection and testing
  • Monoclonal and Polyclonal Antibodies Research
  • Respiratory viral infections research
  • Autophagy in Disease and Therapy
  • Biosensors and Analytical Detection
  • SARS-CoV-2 and COVID-19 Research
  • Cancer-related molecular mechanisms research
  • Virus-based gene therapy research

University of Toledo
2015-2024

University of Kentucky
2024

University of Toledo Medical Center
2017-2024

Medical College and Hospital, Kolkata
2022-2024

Ohio Department of Health
2023

Environmental Protection Agency
2023

Battelle
2023

E Ink (South Korea)
2023

Taylor University
2023

The Ohio State University
2023

TLR3-mediated antiviral responses require phosphorylation of TLR3 by a growth factor receptor and nonreceptor tyrosine kinase.

10.1126/scisignal.2002581 article EN Science Signaling 2012-07-17

ABSTRACT Induction of apoptosis in cells infected by Sendai virus (SeV), which triggers the cytosolic RIG-I pathway, requires presence interferon regulatory factor 3 (IRF-3). Independent IRF-3's transcriptional role, a novel IRF-3 activation pathway causes its interaction with proapoptotic protein Bax and mitochondrial translocation to induce apoptosis. Here we report that two other RNA viruses, vesicular stomatitis (VSV) encephalomyocarditis (EMCV), may also activate same pathway. Moreover,...

10.1128/jvi.02133-10 article EN Journal of Virology 2011-02-10

The interferon (IFN) system represents the first line of defense against a wide range viruses. Virus infection rapidly triggers transcriptional induction IFN-β and IFN Stimulated Genes (ISGs), whose protein products act as viral restriction factors by interfering with specific stages virus life cycle, such entry, transcription, translation, genome replication, assembly egress. Here, we report new mode action an ISG, IFN-induced TDRD7 (tudor domain containing 7) inhibited paramyxovirus...

10.1371/journal.ppat.1006877 article EN cc-by PLoS Pathogens 2018-01-30

Interferon (IFN) regulatory factor 3 (IRF3) is a transcription activated by phosphorylation in the cytoplasm of virus-infected cell; translocating to nucleus, it induces IFN-β and other antiviral genes. We have previously reported IRF3 can also be activated, as proapoptotic factor, its linear polyubiquitination mediated RIG-I pathway. Both transcriptional apoptotic functions contribute effect. Here, we report nontranscriptional function IRF3, namely, repression IRF3-mediated NF-κB activity...

10.1073/pnas.2121385119 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2022-09-06

Here, we report that specific manipulations of the cellular response to virus infection can cause prevention apoptosis and consequent establishment persistent infection. Infection several human cell lines with Sendai (SeV) or parainfluenza 3, two prototypic paramyxoviruses, caused slow apoptosis, which was markedly accelerated upon blocking action phosphatidylinositol 3-kinases (PI3 kinases) in infected cells. The observed required viral gene expression caspase 8 pathway. Although activated...

10.1128/jvi.02536-07 article EN Journal of Virology 2008-01-24

Interferon (IFN) is required for protecting mice from viral pathogenesis; reciprocally, it mediates the deleterious septic shock response to bacterial infection. The critical transcription factor IFN induction, in both cases, IRF-3, which activated by TLR3 or RIG-I signaling virus infection and TLR4 Here, we report that IRF-3's transcriptional activity its coactivators, β-catenin CBP, be modified HDAC6-mediated deacetylation protein kinase C isozyme β (PKC-β)-mediated phosphorylation,...

10.1128/mbio.00636-12 article EN mBio 2013-03-27

Virus-infected cells trigger a robust innate immune response and facilitate virus replication. Here, we review the role of autophagy in infection, focusing on both pro-viral anti-viral host responses using select group viruses. Autophagy is cellular degradation pathway operated at basal level to maintain homeostasis induced by external stimuli for specific functions. The degradative function considered response. However, double-edged sword viral infection; viruses often benefit from it,...

10.3390/immuno2010012 article EN cc-by Immuno 2022-01-30

Interferon (IFN) regulatory factors (IRF) are key transcription in cellular antiviral responses. IRF7, a virus-inducible IRF, expressed primarily myeloid cells, is required for transcriptional induction of IFNα and genes. IRF7 activated by virus-induced phosphorylation the cytoplasm, leading to its translocation nucleus activity. Here, we revealed non-transcriptional activity contributing functions. interacted with pro-inflammatory factor NF-κB-p65 inhibited inflammatory target Using...

10.1016/j.jbc.2024.107200 article EN cc-by-nc-nd Journal of Biological Chemistry 2024-03-18

Abstract TLR3 is one of the major innate immune sensors dsRNA. The signal transduction pathway activated by TLR3, upon binding to dsRNA, leads activation two transcription factors: NF-κB and IFN regulatory factor (IRF) 3. In an effort identify specific chemical modulators TLR3–IRF3 pathway, we developed a cell-based readout system. Using IFN-stimulated gene 56 promoter-driven firefly luciferase stably integrated in TLR3-expressing HEK293 cell line, were able generate line where treatment...

10.4049/jimmunol.0903559 article EN The Journal of Immunology 2010-04-10
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