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Marc Caron, Professor at Duke University Medical Center, to Give Keynote Address on Functional Selectivity at GPCR Structure, Function and Drug Discovery Conference, May 22-23, 2014 in Cambridge, MA

Marc Caron to Give Keynote Address at GPCR Drug Discovery Conference, May 22-23, 2014, Cambridge, MA
    MONROVIA, CA, March 20, 2014 /24-7PressRelease/ -- Dr. Marc Caron, Professor of Cell Biology at the Duke University Medical Center, will give the keynote presentation at the GPCR Structure, Function and Drug Discovery Conference, to be held May 22-23, 2014 in Cambridge, MA.

Dr. Caron, who has focused his research on mechanisms and regulation of G protein-coupled receptors and on the mechanisms of neurotransmission as controlled by neurotransmitter transporters, will speak about "Approaches to Validate and Exploit Functional Selectivity of GPCRs."

Though the recent genomic revolution has provided great hope for identifying disease genes and the development of more selective and efficacious therapies for various human conditions, this hope remains a challenge in the case of psychiatric disorders, in which numerous genetic mutations can lead to similar disease symptoms. Therapeutic agents that target directly or indirectly G protein-coupled receptors (GPCRs) are used to treat many CNS disorder symptoms, with varying degrees of success.

GPCRs can signal not only through G protein activation, but also through the ability of -arrestins to scaffold intracellular signaling molecules with distinct temporal and pharmacological properties. These two signaling modes invariably mediate distinct cellular responses. Thus, agonists and antagonists that can selectively discriminate between these signaling mechanisms may lead to novel, more selective therapeutic agents with fewer side effects. Dr. Caron will share how he and his lab have previously shown that D2 dopamine receptors (D2R), the main target of clinically effective antipsychotics, can engage an Akt/GSK3 signaling pathway via the scaffolding of a -arrestin2/Akt/PP2A/GSK3 complex. In order to further validate the physiological role of this signaling pathway, the lab has used genetic approaches like the neuron selective deletion -arrestin and the downstream GSK3 gene to confirm their mimic of antipsychotic actions.

For more information about this presentation and the conference, please visit

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