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Edward Y. Skolnik, MD

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About Me

Conditions and Treatments

Conditions
  • glomerular disease
  • kidney disease
  • fluids disorder
  • polycystic kidney disease
  • acute renal failure
  • glomerulonephritis
  • kidney failure
  • chronic renal failure
  • high blood pressure disorder
Treatments
  • hemodialysis

Credentials

Positions
  • Professor, Department of Medicine
  • Professor, Department of Biochemistry and Molecular Pharmacology
  • Director, Physician Scientist Medicine Residency Program
Board Certifications
  • American Board of Internal Medicine (Nephrology), 1988
  • American Board of Internal Medicine - Internal Medicine, 1985
Education and Training
  • Fellowship, New York Presbyterian - Weill Cornell Medical Center, Nephrology, 1988
  • Residency, Mount Sinai Medical Center, Medicine, 1985

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Insurance Plans Accepted

This provider accepts the following insurance plans.

  • AETNA INDEMNITY
  • AETNA MEDICARE
  • AETNA POS
  • AETNA PPO/EPO
  • Aetna HMO
  • Empire BC/BS
  • Empire Blue Cross Blue Shield EPO
  • Empire Blue Cross Blue Shield HMO
  • Empire Blue Cross Blue Shield Indemnity
  • Empire Blue Cross Blue Shield MediBlue
  • Empire Blue Cross Blue Shield POS
  • Empire Blue Cross Blue Shield PPO
  • Empire Blue Cross Blue Shield Pathways, Enhanced
  • Fidelis Child Health
  • Fidelis Family Health
  • Fidelis Medicaid
  • GHI
  • GHI HMO
  • HIP ACCESS I
  • HIP ACCESS II
  • HIP Child Health
  • HIP EPO/PPO
  • HIP Family Health
  • HIP HMO
  • HIP MEDICAID
  • HIP MEDICARE
  • HIP POS
  • HealthFirst
  • HealthNet
  • LOCAL 1199 PPO
  • MAGNACARE PPO
  • OSCAR
  • Oxford Freedom
  • Railroad Medicare
  • UnitedHealthcare Community & State Plan
  • UnitedHealthcare EPO
  • UnitedHealthcare HMO
  • UnitedHealthcare Medicare
  • UnitedHealthcare POS
  • UnitedHealthcare PPO
  • UnitedHealthcare Top Tier
View All Accepted Plans This list of insurances changes regularly, and insurance plans listed may not be accepted at all office locations for this provider. Before your appointment, please confirm with your insurance company that this provider accepts your insurance.

Locations and Appointments

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NYU Dialysis Associates

530 1st Avenue, Skirball 9U
New York, NY 10016

NYU Dialysis Associates

560 1st Avenue, 18th Floor
New York, NY 10016

Research My Research

Interests

cancer, channels and transporters, metabolism, pharmacology, signal transduction mechanisms

Research Summary

The Ca2+-activated K+ channel, KCa3.1, is required for Ca2+ influx and the subsequent activation of B and T cells. Inhibitors of KCa3.1 are in development to treat autoimmune diseases and transplant rejection, underscoring the importance in understanding how these channels are regulated. We recently identified several new signaling molecules that are critical for regulating KCa3.1 channel activity in human CD4+ T cells. We found that: 1) the lipid phophatidylinositol 3 phosphate (PI3P) is required for KCa3.1 channel activity and that the PI3P phosphatase, myotubularin related protein 6 (MTMR6) negatively regulates KCa3.1 by dephosphorylating PI3P; 2) Nucleoside Diphosphate Kinase Beta (NDPK-B), a mammalian histidine kinase, is required for KCa3.1 channel activation by phosphorylating histidine (H) 358 in the carboxyl terminus of KCa3.1; and 3) the histidine phosphatase protein histidine phosphatase-1 (PHPT-1) directly binds and dephosphorylates H358 on KCa3.1 leading to KCa3.1 channel inhibition. These findings provide one of the best examples whereby a mammalian histidine kinase and histidine phosphatase regulates a biological process in mammals. Moreover, these studies identify for the first time that NDPK-B is required for activation of a subset of human CD4+ T cells and that MTMR6 and PHPT-1 function to inhibit activation of these cells. We are currently working to understand the mechanism(s) whereby NDPK-B, PHPT-1, and MTMR6 are regulated in CD4+ T cells. These studies should uncover novel pathways that regulate T cell activation and may identify new mechanisms whereby aberrant activation of these pathways can contribute to autoimmune diseases.

Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the presence of innumerous fluid-filled cysts in the kidneys and is a common cause of renal failure. Net fluid secretion into renal cysts is driven by transepithelial Cl- secretion mediated by apical cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channels and is an important factor in kidney enlargement. Our recent studies demonstrated that KCa3.1 also plays a critical role in the regulation of CFTR-mediated Cl- secretion and cyst formation in normal human kidney epithelia (NHK) cells and epithelial cells derived from the cysts of ADPKD kidneys. Moreover, we found that treatment of various mouse models of polycystic kidney disease with the KCa3.1 inhibitor, TRAM34, significantly decreased the formation of cysts in these animals. We currently exploring the use of KCa3.1 inhibitors as a potential new therapy to treat patients with ADPKD.

Academic Contact

Lab Website

Publications

Read All Publications (79)