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John McDonald

Researcher at University of Leicester

Publications -  21
Citations -  668

John McDonald is an academic researcher from University of Leicester. The author has contributed to research in topics: Receptor & 5-HT5A receptor. The author has an hindex of 13, co-authored 21 publications receiving 630 citations.

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Anxiolytic- and antidepressant-like activities of H-Dmt-Tic-NH-CH(CH2-COOH)-Bid (UFP-512), a novel selective delta opioid receptor agonist.

TL;DR: The present findings demonstrate that UFP-512 behaves as a highly potent and selective agonist at Dop receptors and corroborate the proposal that the selective activation of DOP receptors elicits robust anxiolytic- and antidepressant-like effects in rodents.
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Phosphorylation and Regulation of a Gq/11-coupled Receptor by Casein Kinase 1α

TL;DR: The results support the notion that CK1α is able to mediate GPCR phosphorylation in an agonist-dependent manner and that this may provide a novel mechanism for G PCRosphorylation.
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Direct effect of morphine on breast cancer cell function in vitro: role of the NET1 gene

TL;DR: The NET1 gene, but not opioid receptors, is expressed in breast adenocarcinoma cells and may facilitate their migration, implying that NET1 contributes to mediating the direct effect of morphine on breast cancer cell migration.
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Phosphorylation of the Gq/11-coupled m3-muscarinic receptor is involved in receptor activation of the ERK-1/2 mitogen-activated protein kinase pathway.

TL;DR: It is concluded that phosphorylation of the M3-muscarinic receptor on sites in the third intracellular loop by casein kinase 1α contributes to the mechanism of receptor activation of ERK-1/2 by working in concert with the diacylglycerol/PKC arm of the phospholipase C signaling pathway.
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The C-terminal Tail of the M3-muscarinic Receptor Possesses Anti-apoptotic Properties

TL;DR: The anti-apoptotic response of the muscarinic receptor family was confined to the Gq/11-coupled members of this family and the conserved poly-basic region in the C-terminal tail of the M1, M3, and M5 receptors contributes to the ability of these receptors to mediate protection against apoptosis.