M
Marc G. Caron
Researcher at Duke University
Publications - 683
Citations - 104044
Marc G. Caron is an academic researcher from Duke University. The author has contributed to research in topics: Receptor & G protein-coupled receptor. The author has an hindex of 173, co-authored 674 publications receiving 99802 citations. Previous affiliations of Marc G. Caron include United States Department of Veterans Affairs & Tohoku University.
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Journal ArticleDOI
Dopamine Receptors: From Structure to Function
TL;DR: Target deletion of several of these dopamine receptor genes in mice should provide valuable information about their physiological functions and provide unequivocal evidence for the involvement of one of these receptors in the etiology of various central nervous system disorders.
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Hyperlocomotion and indifference to cocaine and amphetamine in mice lacking the dopamine transporter
TL;DR: In homozygote mice, dopamine persists at least 100 times longer in the extracellular space, explaining the biochemical basis of the hyperdopaminergic phenotype and demonstrating the critical role of the transporter in regulating neurotransmission.
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Beta-arrestin-dependent formation of beta2 adrenergic receptor-Src protein kinase complexes.
Louis M. Luttrell,Stephen S. G. Ferguson,Yehia Daaka,William E. Miller,Stuart Maudsley,G. J. Della Rocca,Fang-Tsyr Lin,H. Kawakatsu,K. Owada,D. K. Luttrell,Marc G. Caron,Robert J. Lefkowitz +11 more
TL;DR: Data suggest that beta-arrestin binding, which terminates receptor-G protein coupling, also initiates a second wave of signal transduction in which the "desensitized" receptor functions as a critical structural component of a mitogenic signaling complex.
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Model systems for the study of seven-transmembrane-segment receptors.
TL;DR: This paper presents a meta-analyses of the chiral signaling process and its applications in medicine and animal welfare, and investigates the role of chiral reprograming in the development of Alzheimer's disease.
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Turning off the signal: desensitization of beta-adrenergic receptor function.
TL;DR: The molecular mechanisms underlying rapid βAR desensitization do not appear to require internalization of the receptors, but rather an alteration in the functioning of βAR themselves that uncouples the receptors from the stimulatory G protein Gs.