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Satpal                         Singh

Satpal Singh PhD

Department of Pharmacology and Toxicology

Professor

Specialty/Research Focus

Behavioral pharmacology; Cardiac pharmacology; Ion channel kinetics and structure; Membrane Transport (Ion Transport); Molecular Basis of Disease; Neurobiology; Neuropharmacology; Signal Transduction; Transgenic organisms

 
Professional Summary:

With over 400 genes coding for them in humans, ion channels play a significant role in most physiological functions. Drug-induced channel dysfunction often leads to a variety of disorders and results in significant incidence of serious injury and death. We investigate molecular mechanisms underlying neurodegenerative disorders and cardiac arrhythmias induced by ion channel dysfunction arising from genetic factors and/or drug interactions. The tools used for these investigations include genetic, electrophysiologic, pharmacologic, molecular and cell culturing methods. Preparations used for experiments include Drosophila as a genetic model system, and human cell lines expressing human ion channels that play an important role in critical-to-life functions including cardiac rhythm, respiration and the central nervous system.

Education and Training:
  • PhD, Molecular Biology, Tata Institute of Fundamental Research, Bombay, India (1980)
  • MS, Physics, Punjab University, Chandigarh, India, Honors (1973)
  • BS, Physics, Punjab University, Chandigarh, India, Honors (1972)
Employment:
  • Associate Professor, Biochemical Pharmacology/Pharmacology & Toxicology, State University of New York at Buffalo (1997-present)
  • Assistant Professor, State University of New York at Buffalo (1989–1997)
  • Visiting Associate Professor, Department of Biology, University of Iowa (1989)
  • Assistant Professor, Department of Biology, Guru Nanak Dev (G.N.D.) University (1982–1985)

Research Expertise:
  • Channelopathies: With over 400 genes coding for them in humans, ion channels play a significant role in most physiological functions. Drug-induced channel dysfunction often leads to a variety of disorders and results in significant incidence of serious injury and death. We investigate molecular mechanisms underlying neurodegenerative disorders and cardiac arrhythmias induced by ion channel dysfunction arising from genetic factors and/or drug interactions. The tools used for these investigations include genetic, electrophysiologic, pharmacologic, molecular and cell culturing methods. Preparations used for in experiments include Drosophila as a genetic model system, and human cell lines expressing human ion channels that play an important role in critical-to-life functions including cardiac rhythm, respiration and the central nervous system.
UB 2020 Strategic Strengths:
  • Molecular Recognition in Biological Systems and Bioinformatics
  • Health and Wellness Across the Lifespan
Grants and Sponsored Research:
  • September 2011–August 2016
    Targeted MSP: The University at Buffalo/Buffalo Public Schools (UB/BPS) Interdisciplinary Science and Engineering Partnership
    National Science Foundation
    Role: Co-Investigator
    $9,831,207
  • July 2010–June 2013
    Subcontract for Science support for NY State Ed Math Science Partnership - Buffalo Public Schools
    New York State Department of Education
    Role: Co-Investigator
    $254,976
  • August 2008–September 2011
    A Genetic Model of Leigh Syndrome Suppression in Drosophila
    NIH (NINDS)
    Role: Principal Investigator
    $158,500
  • January 2006–December 2009
    Interdisciplinary Science Research-based Curricular Innovations for Middle and High School Science and Teacher Professional Development
    John R. Oishei Foundation
    Role: Co-Investigator
    $480,000

Journal Articles:
See all (24 more)
Abstracts:
  • Chopra, M., Gu, G.-G. and Singh, S. Mutations Affecting the Delayed Rectifier Potassium Current in Drosophila. J. Neurogenetics. ; 14.
  • Hedge, P., Gu, G-G., Chen, D., Free, S.J. and Singh, S.. Mutational Analysis of the Shab-encoded Delayed Rectifier K+ channels in Drosophila. J. Biol. Chem.. ; 274.
  • Singh, A. and Singh, S.. Unmasking of a Novel Potassium Current in Drosophila by a Mutation and Drugs. J. Neurosci.. ; 19.
  • Bhattacharya, A., Gu., G.-G. and Singh, S.. Modulation of the Dihydropyridine-Sensitive Calcium Channels in Drosophila by a cAMP-Mediated Pathway. J. Neurobiol.. ; 39.
  • Kraliz, D., Bhattacharya, A. and Singh, S.. Blockade of the Delayed Rectifier Potassium Current in Drosophila by Quinidine and Related Compounds. J. Neurogenet.. ; 12.
  • Gu G.-G. and Singh, S.. Modulation of the dihydropyridine-sensitive Ca2+ channels in Drosophila by a phospholipase C-mediated pathway. J. Neurobiology. ; 33.
  • Kraliz, D. and Singh, S.. Selective Blockade of the delayed rectifier potassium current by tacrine in Drosophila. J. Neurobiology. ; 32.
  • Gielow, M.L., Gu, G.-G. and Singh, S.S.. Resolution and pharmacological analysis of the voltage-dependent calcium channels of Drosophila larval muscles. J. Neuroscience. ; 15.
  • Satpal Singh. Pharmacological analysis of heartbeat in Drosophila. j. Neurobiology. ; 28.
  • Chopra, M. and Singh, S.. Developmental temperature selectively regulates a voltage-activated potassium current in Drosophila. J. Neurobiol.. ; 25.
  • Komatsu, A., K., Singh, S., Rathe, P. and Wu, C.-F.. Mutational and gene-dosage analysis of calcium-activated potassium channels in Drosophila: Correlation of micro- and macroscopic currents. Neuron. ; 4.
  • Singh, S. and Wu, C.-F.. Properties of potassium currents and their role in membrane excitability in Drosophila larval muscle fibers. J. Exp. Biol.. ; 152.
  • Wu, C.-F., Tsai, M.-C., Chen, M.-L., Zhong, Y., Singh, S. and Lee, C.Y.. Actions of dendrotoxin on K+ channels and neuromuscular transmission in Drosophila melanogaster and its effects in synergy with K+ channel-specific drugs and mutations. J. Exp. Biol.. ; 147.
  • Singh, S., Bhandari, P., Chopra, M.J.S. and Guha, D.. Isolation of autosomal mutations in Drosophila melanogaster without setting up lines. Molec. Gen. Genet.. ; 208.
  • Singh, S.. A mutagenesis scheme for obtaining autosomal mutations in Drosophila. Ind. J. Exp. Biol.. ; 21.
  • Singh, S. and Siddiqi, O.. Torpid, a new sex linked temperature paralytic mutation in Drosophila melanogaster. Molec. Gen. Genet.. ; 181.
See all (6 more)


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Contact Information

206 Cary Hall
Buffalo, NY 14214
Phone: (716) 829-2453
Fax: (716) 829-2801
Email: singhs@buffalo.edu


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