Piyali Mukherjee

ORCID: 0000-0002-0140-7414
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About
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Research Areas
  • interferon and immune responses
  • Immune Response and Inflammation
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Viral Infections and Vectors
  • Sirtuins and Resveratrol in Medicine
  • Autophagy in Disease and Therapy
  • Mosquito-borne diseases and control
  • Calcium signaling and nucleotide metabolism
  • Viral Infections and Immunology Research
  • NF-κB Signaling Pathways
  • Viral-associated cancers and disorders
  • Herpesvirus Infections and Treatments
  • Vector-Borne Animal Diseases
  • Inflammasome and immune disorders
  • Parvovirus B19 Infection Studies
  • RNA regulation and disease
  • Cytomegalovirus and herpesvirus research
  • MicroRNA in disease regulation
  • RNA Interference and Gene Delivery
  • Parkinson's Disease Mechanisms and Treatments
  • Nerve injury and regeneration

Presidency University
2018-2022

Presidency University
2021

National Institute of Allergy and Infectious Diseases
2013-2015

National Institutes of Health
2012-2015

Abstract Neuronal apoptosis is a key aspect of many different neurologic diseases, but the mechanisms remain unresolved. Recent studies have suggested mechanism innate immune-induced neuronal through stimulation endosomal TLRs in neurons. are stimulated both by pathogen-associated molecular patterns as well damage-associated patterns, including microRNAs released damaged In present study, we identified responsible for TLR7/TLR9-mediated apoptosis. TLR-induced required localization was...

10.4049/jimmunol.1500953 article EN The Journal of Immunology 2015-10-01

Latent EBV infection is causally associated with various B-cell malignancies, while periodic lytic-cycle replication essential for sustaining viral progeny. Lytic cycle induction represents a promising therapeutic strategy EBV-associated neoplasms. Therefore, uncovering the mechanisms that regulate reactivation pivotal understanding pathogenesis and advancing novel therapies. Our genome-wide transcriptomic analysis reveals E2F1 expression transcriptionally activated during latent in...

10.1101/2025.01.23.634435 preprint EN cc-by bioRxiv (Cold Spring Harbor Laboratory) 2025-01-26

Rotenone, a lipophilic pesticide, is strongly linked to dopaminergic neuronal loss in Parkinsons disease (PD), primarily through mitochondrial complex I inhibition. While rotenone induces G2/M arrest dividing cells, the underlying molecular events remain unclear. We identify HMGB1 as key player this process. HMGB1, known for its roles genomic integrity and inflammation, exits nucleus during rotenone-induced arrest, whereas nuclear retention protects against mitotic DNA damage. further reveal...

10.1101/2025.03.25.645152 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2025-03-26

The activation of astrocytes and microglia is often associated with diseases the central nervous system (CNS). Understanding how alters transcriptome these cells may offer valuable insight regarding mediate neurological damage. Furthermore, identifying common unique pathways gene expression during provide new into distinct roles have in CNS infection inflammation. Since recent studies indicate that TLR7 recognizes not only viral RNA but also microRNAs are released by damaged neurons elevated...

10.1371/journal.pone.0127336 article EN public-domain PLoS ONE 2015-07-27

Toll-like receptor 7 (TLR7) recognizes guanidine-rich viral ssRNA and is an important mediator of peripheral immune responses to several viruses. However, the role that TLR7 plays in regulating innate response virus infections specific organs such as central nervous system (CNS) not clear. This study examined influence on neurovirulence Langat (LGTV), a tick-borne flavivirus. deficiency did substantially alter onset or incidence LGTV-induced clinical disease; however, it significantly affect...

10.1099/vir.0.043984-0 article EN Journal of General Virology 2012-11-08

Aging is a complex biological process and environmental risk factors like pesticide exposure have been implicated in the increased incidence of age-related neurodegenerative diseases Parkinson's disease (PD) but etiology remains unknown. There also lack proper animal model system to study progressive effect these toxins on age-associated neurodegeneration. In this study, we established drosophila aging age-dependent vulnerability toxin rotenone that has sporadic cases PD. We demonstrate age...

10.1038/s41420-018-0119-5 article EN cc-by Cell Death Discovery 2018-12-11

Sarm1 is an evolutionary conserved innate immune adaptor protein that has emerged as a primary regulator of programmed axonal degeneration over the past decade. In vitro structural insights have revealed although induces energy depletion by breaking down nicotinamide adenine dinucleotide+ (NAD+ ), it also allosterically inhibited NAD+ . However, how levels modulate activation intracellular not been elucidated so far. This study focuses on understanding events leading to in both neuronal and...

10.1111/febs.16652 article EN FEBS Journal 2022-10-14

Abstract Sarm1 is an evolutionary conserved innate immune adaptor protein that has emerged as a primary regulator of programmed axonal degeneration over the past decade. In vitro structural insights have revealed although induces energy depletion by breaking down NAD + , it also allosterically inhibited . However, how levels modulate activation intracellular not been elucidated so far. This study focuses on understanding events leading to in both neuronal and non-neuronal cells using...

10.1101/2021.07.30.454548 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2021-07-31

Abstract Neuronal cell death is a hallmark of various neurological diseases including virus infection. The innate immune response in the CNS contributes to neuronal damage through cytokine and neurotoxin production as well recruitment inflammatory cells. However, role induction poorly understood. La Crosse (LACV), which major cause pediatric encephalitis United States, predominantly infects neurons associated with neurodegenerative changes. Infection results apoptosis. In current studies we...

10.4049/jimmunol.188.supp.170.2 article EN The Journal of Immunology 2012-05-01
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