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Pradipta Ghosh

Pradipta Ghosh

· Professor

University of California, San Diego · Cellular and Molecular Medicine

Active 1994–2026

h-index47
Citations7.6k
Papers301170 last 5y
Funding$31.2M3 active

Academic metrics are sourced from OpenAlex and public funding records; values may differ from Google Scholar.

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About

Dr. Pradipta Ghosh is an Indian-born American physician-scientist, biochemist, and cell biologist with dual expertise in clinical medicine and basic research. She is a Professor in the Departments of Medicine and Cellular & Molecular Medicine at the University of California, San Diego, where she leads an innovative research group focused on cellular communication networks. Her pioneering work has significantly advanced the understanding of how intracellular heterotrimeric G-proteins are regulated by a novel family of guanine-nucleotide exchange modulators (GEMs), independently of traditional G-protein-coupled receptors (GPCRs). This groundbreaking research has uncovered new mechanisms of cell signaling with important implications for chronic diseases such as cancer, fibrosis, immunologic, and metabolic disorders. Ghosh's contributions have provided key insights into how intracellular communication is disrupted in disease, representing a conceptual breakthrough after prior attempts to unravel this network had failed. Recognizing the need for innovative tools to probe the laws governing cellular function, Dr. Ghosh founded the Institute for Network Medicine in 2018. This institute houses four transdisciplinary centers that synergistically work to uncover the unifying principles of cellular behavior, also known as invariants. These centers employ computational approaches, 3D cultures of human organoids and primary cells, advanced cell analysis techniques, and systems…

Research topics

  • Biology
  • Cell biology
  • Medicine
  • Computer Science
  • Immunology
  • Computational biology
  • Biochemistry
  • Chemistry
  • Data science
  • Neuroscience

Selected publications

  • Adult stem cell-derived complete lung organoid models emulate lung disease in COVID-19

    eLife · 2021 · 131 citations

    Background: SARS-CoV-2, the virus responsible for COVID-19, causes widespread damage in the lungs in the setting of an overzealous immune response whose origin remains unclear. Methods: We present a scalable, propagable, personalized, cost-effective adult stem cell-derived human lung organoid model that is complete with both proximal and distal airway epithelia. Monolayers derived from adult lung organoids (ALOs), primary airway cells, or hiPSC-derived alveolar type II (AT2) pneumocytes were inf…

  • Drug repurposing screens identify chemical entities for the development of COVID-19 interventions

    Nature Communications · 2021 · 127 citations

    The ongoing pandemic caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), necessitates strategies to identify prophylactic and therapeutic drug candidates for rapid clinical deployment. Here, we describe a screening pipeline for the discovery of efficacious SARS-CoV-2 inhibitors. We screen a best-in-class drug repurposing library, ReFRAME, against two high-throughput, high-content imaging infection assays: one using HeLa cells expressing SARS-CoV-2 receptor ACE2 and…

  • TLR4 signaling and macrophage inflammatory responses are dampened by GIV/Girdin

    Proceedings of the National Academy of Sciences · 2020 · 103 citations

    Senior authorCorresponding

    Sensing of pathogens by Toll-like receptor 4 (TLR4) induces an inflammatory response; controlled responses confer immunity but uncontrolled responses cause harm. Here we define how a multimodular scaffold, GIV (a.k.a. Girdin), titrates such inflammatory response in macrophages. Upon challenge with either live microbes or microbe-derived lipopolysaccharides (a ligand for TLR4), macrophages with GIV mount a more tolerant (hypo-reactive) transcriptional response and suppress proinflammatory cytokin…

  • MDA5-autoimmunity and interstitial pneumonitis contemporaneous with the COVID-19 pandemic (MIP-C)

    EBioMedicine · 2024-05-08 · 37 citations

    articleOpen access

    BACKGROUND: -DM) is characterised by rapidly progressive interstitial lung disease (ILD) and high mortality. MDA5 is an RNA sensor and a key pattern recognition receptor for the SARS-CoV-2 virus. METHODS: -DM outbreak. FINDINGS: Sixty new anti-MDA5+, but not other MSAs surged between 2020 and 2022, increasing from 0.4% in 2019 to 2.1% (2020), 4.8% (2021) and 1.7% (2022). Few (8/60) had a prior history of confirmed COVID-19, peak rates overlapped with regional SARS-COV-2 community positivity rate…

  • Receptor tyrosine kinases activate heterotrimeric G proteins via phosphorylation within the interdomain cleft of Gαi

    Proceedings of the National Academy of Sciences · 2020 · 36 citations

    Senior authorCorresponding

    The molecular mechanisms by which receptor tyrosine kinases (RTKs) and heterotrimeric G proteins, two major signaling hubs in eukaryotes, independently relay signals across the plasma membrane have been extensively characterized. How these hubs cross-talk has been a long-standing question, but answers remain elusive. Using linear ion-trap mass spectrometry in combination with biochemical, cellular, and computational approaches, we unravel a mechanism of activation of heterotrimeric G proteins by…

Recent grants

Frequent coauthors

  • Debashis Sahoo

    University of California, San Diego

    122 shared
  • Amer Ali Abd El‐Hafeez

    Children Cancer Hospital

    82 shared
  • Soumita Das

    University of Massachusetts Lowell

    78 shared
  • Jason Ear

    California State Polytechnic University

    49 shared
  • Ibrahim M. Sayed

    University of Massachusetts Lowell

    40 shared
  • Nicolas Aznar

    Centre National de la Recherche Scientifique

    40 shared
  • Gajanan D. Katkar

    University of California, San Diego

    38 shared
  • Saptarshi Sinha

    University of California, San Diego

    35 shared

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