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Graeme Milligan

Researcher at University of Glasgow

Publications -  570
Citations -  32250

Graeme Milligan is an academic researcher from University of Glasgow. The author has contributed to research in topics: Receptor & G protein. The author has an hindex of 88, co-authored 556 publications receiving 30032 citations. Previous affiliations of Graeme Milligan include University of Leicester & Autonomous University of Barcelona.

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Differential capacities of the RGS1, RGS16 and RGS–GAIP regulators of G protein signaling to enhance α2A‐adrenoreceptor agonist‐stimulated GTPase activity of Go1α

TL;DR: It is demonstrated that RGS1, RGS16 and RGS–GAIP show a high degree of selectivity to regulate α2A‐adrenoreceptor‐activated Go1α rather than Gi1α, Gi2α or Gi3α and different capacities to inactivate this G’protein.
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Roundabout 1 exists predominantly as a basal dimeric complex and this is unaffected by binding of the ligand Slit2.

TL;DR: Combinations of both autofluorescent protein-based FRET imaging and time-resolved FRET were employed and identified oligomeric organization of Robo1 that did not require the presence of the intracellular domain.
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Alterations in G-protein expression and the hormonal regulation of adenylate cyclase in the adipocytes of obese (fa/fa) Zucker rats.

TL;DR: It is suggested that the attenuated activation of adenylate cyclase by stimulatory ligands in membranes from obese animals may be caused by decreases in both Gs and receptors, and that this may contribute to the attenuates lipolytic response seen in adipocytes from such animals.
Journal Article

Differential Uncoupling of A1 Adenosine and D2 Dopamine Receptors by Suramin and Didemethylated Suramin (NF037)

TL;DR: The affinity of the receptors for rGi alpha-1 is inversely correlated with the potency of suramin in uncoupling ternary complexes formed by these receptors and thus determines the selectivity of the suramin analogues for specific receptor/G protein tandems.
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Resolution of Inverse Agonist-Induced Up-Regulation from Constitutive Activity of Mutants of the α1b-Adrenoceptor

TL;DR: The results demonstrate the nonequivalence of mutations in their regulation by antagonist/inverse agonist ligands in the hamster alpha(1b)-adrenoceptor and a mutant lacking eight serine residues in the C-terminal tail that displayed little constitutive activity but was up-regulated by sustained ligand challenge.