about
Agonist-selective, receptor-specific interaction of human P2Y receptors with beta-arrestin-1 and -2Phosphorylation of GRK2 by protein kinase C abolishes its inhibition by calmodulin.FRET-based detection of M1 muscarinic acetylcholine receptor activation by orthosteric and allosteric agonists.μ-opioid receptors: correlation of agonist efficacy for signalling with ability to activate internalization.Dual single-scission event analysis of constitutive transferrin receptor (TfR) endocytosis and ligand-triggered β2-adrenergic receptor (β2AR) or Mu-opioid receptor (MOR) endocytosis.The GIP receptor displays higher basal activity than the GLP-1 receptor but does not recruit GRK2 or arrestin3 effectively.Endomorphin-2: a biased agonist at the μ-opioid receptor.A reverse signaling pathway downstream of Sema4A controls cell migration via Scrib.SK2 channels regulate mitochondrial respiration and mitochondrial Ca2+ uptake.Identification of key phosphorylation sites in PTH1R that determine arrestin3 binding and fine-tune receptor signalingBeta-arrestin binding to the beta2-adrenergic receptor requires both receptor phosphorylation and receptor activation.The amino-terminal domain of G-protein-coupled receptor kinase 2 is a regulatory Gbeta gamma binding site.Morphine-induced internalization of the L83I mutant of the rat μ-opioid receptorMutations of Tyr326 in the beta 2-adrenoceptor disrupt multiple receptor functions.Engineered hyperphosphorylation of the β2-adrenoceptor prolongs arrestin-3 binding and induces arrestin internalization.Dual regulation of the parathyroid hormone (PTH)/PTH-related peptide receptor signaling by protein kinase C and beta-arrestins.Mutation of Asn293 to Asp in transmembrane helix VI abolishes agonist-induced but not constitutive activity of the beta(2)-adrenergic receptor.Evidence that GABA rho subunits contribute to functional ionotropic GABA receptors in mouse cerebellar Purkinje cells.Influence of gαq on the dynamics of m3-acetylcholine receptor-g-protein-coupled receptor kinase 2 interaction.Genetic Expression of an Amyloid Peptide Fragment and Analysis of Formylated ProductsG-protein-coupled receptor kinasesKinetics of G-protein-coupled receptor signalling and desensitizationPeptide inhibitors of G protein-coupled receptor kinasesMultisite phosphorylation is required for sustained interaction with GRKs and arrestins during rapid μ-opioid receptor desensitizationLow intrinsic efficacy for G protein activation can explain the improved side effect profiles of new opioid agonistsA Dual GLP-1/GIP Receptor Agonist Does Not Antagonize Glucagon at Its Receptor but May Act as a Biased Agonist at the GLP-1 ReceptorCorrection: Al-Zamel, N., et al. A Dual GLP-1/GIP Receptor Agonist Does Not Antagonize Glucagon at Its Receptor but May Act as a Biased Agonist at the GLP-1 Receptor. Int. J. Mol. Sci. 2019, 20, 3532
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description
onderzoeker
@nl
researcher
@en
հետազոտող
@hy
name
Cornelius Krasel
@ast
Cornelius Krasel
@en
Cornelius Krasel
@es
Cornelius Krasel
@nl
Cornelius Krasel
@sl
type
label
Cornelius Krasel
@ast
Cornelius Krasel
@en
Cornelius Krasel
@es
Cornelius Krasel
@nl
Cornelius Krasel
@sl
prefLabel
Cornelius Krasel
@ast
Cornelius Krasel
@en
Cornelius Krasel
@es
Cornelius Krasel
@nl
Cornelius Krasel
@sl
P106
P31
P496
0000-0001-8309-8696