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  • photo of neurobiology associate professor paul whiteaker

    Paul Whiteaker, PhD

    Professor, Neurobiology
    (602) 406-6534

    Dr. Paul Whiteaker has over two decades of experience working in nicotinic acetylcholine receptor research. He has provided original insights that have helped to define the subunit composition and functional and ligand-binding pharmacology of naturally expressed nicotinic receptor subtypes.

    More recently, he has established a research program to recapitulate the diversity of naturally expressed nicotinic receptors using heterologous expression systems. This research background has provided Dr. Whiteaker with a wealth of experience in devising, exploiting, and publishing on novel nicotinic model systems, pharmacological agents, and assays. Current areas of focus are mutually supporting and include receptor structure and function studies, development of novel pharmacological reagents (with a particular emphasis on highly selective peptides derived from naturally occurring α-conotoxin ligands), and development of high throughput-capable assays. The resulting insights and reagents will be used to probe the roles of nicotinic receptors in normal and disease physiological processes, and to identify novel pharmacotherapeutic possibilities.

    Dr. Whiteaker is a graduate of the University of Bath, in the United Kingdom. He performed postdoctoral training at the University of Colorado – Boulder before joining the faculty at Barrow Neurological Institute in 2008, where he is an associate professor.

    Education & Training
    • Wellcome Trust Postdoctoral Fellowship, University of Bath, UK, 1997
    • PhD, University of Bath, UK, Biochemistry, 1996
    • BSc, University of Bath, UK, Biochemistry with honors, 1992
    Professional Memberships
    • Barrow – ASU Interdisciplinary Graduate Program in Neuroscience Executive Committee
    • Grant Reviewer, NIH NPAS, PMDA Study Sections
    • Grant Reviewer, California Tobacco-Related Disease Research Program (TRDRP) Nicotine Dependence Study Section
    • Society for Neuroscience
    • American Society for Pharmacology and Experimental Therapeutics
    • Ad hoc reviewer, multiple journals, including: Biochemistry, Brain Research, British Journal of Pharmacology, European Journal of Pharmacology, Journal of Pharmacology and Experimental Therapeutics, Molecular Pharmacology, PLOS ONE, Nicotine and Tobacco Research
    Selected Publications

    View complete list of publications on PubMed.

    1. Moretti M, Zoli M, George AA, Lukas RJ, Pistillo F, Maskos U, Whiteaker P, Gotti C. The novel alpha7beta2-nicotinic acetylcholine receptor subtype is expressed in mouse and human basal forebrain: biochemical and pharmacological characterization. Mol Pharmacol. Sep 2014;86(3):306-317.
    2. Marks MJ, Grady SR, Salminen O, Paley MA, Wageman CR, McIntosh JM, Whiteaker P. alpha6beta2*-subtype nicotinic acetylcholine receptors are more sensitive than alpha4beta2*-subtype receptors to regulation by chronic nicotine administration. J Neurochem. Jul 2014;130(2):185-198.
    3. Luo S, Zhangsun D, Schroeder CI, Zhu X, Hu Y, Wu Y, Weltzin MM, Eberhard S, Kaas Q, Craik DJ, McIntosh JM, Whiteaker P. A novel alpha4/7-conotoxin LvIA from Conus lividus that selectively blocks alpha3beta2 vs. alpha6/alpha3beta2beta3 nicotinic acetylcholine receptors. FASEB J. Apr 2014;28(4):1842-1853.
    4. Eaton JB, Lucero LM, Stratton H, Chang Y, Cooper JF, Lindstrom JM, Lukas RJ, Whiteaker P. The unique alpha4+/-alpha4 agonist binding site in (alpha4)3(beta2)2 subtype nicotinic acetylcholine receptors permits differential agonist desensitization pharmacology versus the (alpha4)2(beta2)3 subtype. J Pharmacol Exp Ther. Jan 2014;348(1):46-58.
    5. George AA, Lucero LM, Damaj MI, Lukas RJ, Chen X, Whiteaker P. Function of human alpha3beta4alpha5 nicotinic acetylcholine receptors is reduced by the alpha5(D398N) variant. J Biol Chem. Jul 20 2012;287(30):25151-25162.
    6. Whiteaker P, Marks MJ, Christensen S, Dowell C, Collins AC, McIntosh JM. Synthesis and characterization of 125I-alpha-conotoxin ArIB[V11L;V16A], a selective alpha7 nicotinic acetylcholine receptor antagonist. J Pharmacol Exp Ther. Jun 2008;325(3):910-919.
    7. Whiteaker P, Cooper JF, Salminen O, Marks MJ, McClure-Begley TD, Brown RW, Collins AC, Lindstrom JM. Immunolabeling demonstrates the interdependence of mouse brain alpha4 and beta2 nicotinic acetylcholine receptor subunit expression. J Comp Neurol. Dec 20 2006;499(6):1016-1038.
    8. Gotti C, Moretti M, Clementi F, Riganti L, McIntosh JM, Collins AC, Marks MJ, Whiteaker P. Expression of nigrostriatal alpha 6-containing nicotinic acetylcholine receptors is selectively reduced, but not eliminated, by beta 3 subunit gene deletion. Mol Pharmacol. Jun 2005;67(6):2007-2015.
    9. Whiteaker P, Peterson CG, Xu W, McIntosh JM, Paylor R, Beaudet AL, Collins AC, Marks MJ. Involvement of the alpha3 subunit in central nicotinic binding populations. J Neurosci. Apr 1 2002;22(7):2522-2529.
    10. Whiteaker P, McIntosh JM, Luo S, Collins AC, Marks MJ. 125I-alpha-conotoxin MII identifies a novel nicotinic acetylcholine receptor population in mouse brain. Mol Pharmacol. May 2000;57(5):913-925.

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