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Professor of
Medicine
Director, Molecular Pharmacology Research Center
Molecular Cardiology Research Institute
Tufts New England Medical Center Hospital
15 Kneeland Street, 7th floor
Boston, MA 02111
Phone: (617) 636-4834
Fax: (617) 636-8692
Email: akopin@tufts-nemc.org
For the most recent description of Dr. Kopin's research and citations,
please click on
Dr. Kopin's Lab Page:
http://160.109.101.132/mcri/MCRILabs/MolecularPharmacologyResearchCenter/default
Research Interests:
Research interests of the Kopin laboratory include exploring the
molecular basis of metabolic (obesity, diabetes) and neurologic
(Parkinson’s) disorders. Current studies focus on: (i) the
role of G protein-coupled receptors (GPCRs) in modulating metabolic
function as well as locomotor activity and (ii) the identification
and characterization of disease relevant genes using Drosophila
as a model system.
Ongoing structure-function studies of GPCRs are aimed at defining
surrogate ligands as molecular/functional probes, determining the
pharmacologic and physiologic consequences of protein coding polymorphisms,
and further exploring the molecular basis/utility of constitutively
active receptors. As research tools, we combine in vitro cell based
assays with in vivo models (e.g. knockout mice, transgenic Drosophila,
recombinant protein expression using viral vectors). Receptor families
of particular interest include CCK/gastrin, melanocortin, dopamine,
serotonin, and GABA.
In addition, we are screening Drosophila mutants to identify novel
genes mediating feeding behavior, fat deposition, and abnormalities
in locomotor activity. Candidate genes that have corresponding mammalian
homologs are prioritized for further characterization. These studies
may expedite the identification of genes which underlie susceptibility
to metabolic or neurologic disorders.
Recent Publications:
1. Locomotor activity is regulated by D2-like receptors in Drosophila: An anatomic and functional analysis. Developmental Neurobiology. 2007 Feb.
2. Identification of Amino Acid Determinants of Dopamine 2 Receptor Synthetic Agonist Function. Journal of Pharmacology and Experimental Therapeutics. 2007 Jan.
3. Four Missense Mutations in the Ghrelin Receptor Result in Distinct Pharmacological Abnormalities. Journal Pharmacology Experimental Therapeutics 322(3):1036-1043, 2007. PubMed Abstract
4. Identification of a series of CCK-2 receptor nonpeptide agonists: Sensitivity to stereochemistry and a receptor point mutation. Proceedings of the National Academy of Sciences, USA. 2003 Apr.
5. CCK receptor polymorphisms: an illustration of emerging themes in pharmacogenomics. Trends in Pharm. Sciences. 21(9):319-359, 2000. PubMed Abstract
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