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Edward Y. Skolnik

· Professor

New York University · Cell Biology

Active 1943–2026

h-index67
Citations20.9k
Papers1353 last 5y
Funding$8.3M

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

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About

Edward Y. Skolnik, MD, is a professor in the Department of Cell Biology and the Department of Medicine at NYU Grossman School of Medicine. His research focuses on the physiology and immunology of ion channels, particularly the Ca2+-activated K+ channel, KCa3.1, which is essential for Ca2+ influx and the activation of B and T cells. He has identified several signaling molecules that regulate KCa3.1 activity in human CD4+ T cells, including the lipid phosphatidylinositol 3 phosphate (PI3P), the PI3P phosphatase MTMR6, the mammalian histidine kinase NDPK-B, and the histidine phosphatase PHPT-1. His work demonstrates how these molecules influence T cell activation and may contribute to autoimmune diseases. Dr. Skolnik's research also extends to kidney disease, particularly autosomal dominant polycystic kidney disease (ADPKD). His studies have shown that KCa3.1 plays a critical role in regulating CFTR-mediated chloride secretion and cyst formation in kidney epithelia. He has demonstrated that KCa3.1 inhibitors, such as TRAM34, can significantly decrease cyst formation in mouse models of polycystic kidney disease, exploring the potential of these inhibitors as a new therapy for ADPKD. His work combines cellular physiology, signal transduction, and pharmacology to uncover novel pathways involved in immune regulation and kidney disease.

Research topics

  • Medicine
  • Internal medicine
  • Endocrinology
  • Physics
  • Biology
  • Urology
  • Surgery
  • Biotechnology

Selected publications

  • Glutamine metabolism via glutaminase 1 in autosomal-dominant polycystic kidney disease

    Nephrology Dialysis Transplantation · 2017-12-06 · 40 citations

    articleOpen accessSenior author

    Background: Metabolism of glutamine by glutaminase 1 (GLS1) plays a key role in tumor cell proliferation via the generation of ATP and intermediates required for macromolecular synthesis. We hypothesized that glutamine metabolism also plays a role in proliferation of autosomal-dominant polycystic kidney disease (ADPKD) cells and that inhibiting GLS1 could slow cyst growth in animal models of ADPKD. Methods: Primary normal human kidney and ADPKD human cyst-lining epithelial cells were cultured in…

  • Regulation of KATP Channel Trafficking in Pancreatic β-Cells by Protein Histidine Phosphorylation

    Diabetes · 2018-02-12 · 25 citations

    articleOpen accessSenior authorCorresponding

    Protein histidine phosphatase 1 (PHPT-1) is an evolutionarily conserved 14-kDa protein that dephosphorylates phosphohistidine. PHPT-1−/− mice were generated to gain insight into the role of PHPT-1 and histidine phosphorylation/dephosphorylation in mammalian biology. PHPT-1−/− mice exhibited neonatal hyperinsulinemic hypoglycemia due to impaired trafficking of KATP channels to the plasma membrane in pancreatic β-cells in response to low glucose and leptin and resembled patients with congenital hy…

  • Physiology and immunology of a pig-to-human decedent kidney xenotransplant

    Nature · 2025-11-13 · 16 citations

    article
  • Multi-omics analysis of a pig-to-human decedent kidney xenotransplant

    Nature · 2025-11-13 · 13 citations

    articleOpen access
  • Xenotransplantation

    Journal of the American Society of Nephrology · 2025-04-16 · 7 citations

    articleOpen access

    The scarcity of transplantable organs represents a worldwide public health crisis, and as a result, thousands of people with kidney failure die waiting for a transplant each year. Xenotransplantation involves transplanting organs from an animal source into humans, offering a potential solution to this significant unmet need. Indeed, if there is a limitless supply of organs, many more patients who do not meet the current criteria for transplant eligibility could also be considered as candidates.…

Recent grants

Frequent coauthors

  • Li Zhai

    Blagoveschensk State Pedagogical University

    96 shared
  • Thomas Wieland

    University Medical Centre Mannheim

    91 shared
  • Yi Hua Qiu

    The University of Texas MD Anderson Cancer Center

    82 shared
  • Yuxi Feng

    Yangzhou University

    82 shared
  • Dobromir Dobrev

    Montreal Heart Institute

    73 shared
  • Katharina Spiger

    University Hospital Heidelberg

    73 shared
  • Martin Borggrefe

    University Medical Centre Mannheim

    64 shared
  • Xiaobo Zhou

    Zhejiang Taizhou Hospital

    64 shared

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