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Bioorganic & medicinal chemistry letters, 08/2019, pp. 126611 - 126611
Journal Article
Tetrahedron, ISSN 0040-4020, 01/2019, Volume 75, Issue 2, pp. 286 - 295
A panel of three lipid-modified, functionalized biphenyl cross-linkers (fBph) were synthesized and subsequently employed in the preparation of the stapled... 
Oxyntomodulin | Dual agonist | Cross-linker | GCGR | GLP-1R | POTENT | PEPTIDES | CHEMISTRY, ORGANIC | GLP-1 ANALOG | INHIBITORS
Journal Article
11/2009
G-protein coupled receptors (GPCRs) have been shown to act as part of GPCR associated protein complexes (GAPCs) which are required to appropriately transduce... 
0369 | GLP-1 | GIPR | GCGR | 0719 | glucagon | GPCR | protein-protein interaction | 0307 | B class GCPR | GLP-2R
Dissertation
Molecular Metabolism, ISSN 2212-8778, 11/2018, Volume 17, pp. 28 - 38
Mice with congenital loss of the glucagon receptor gene ( mice) remain normoglycemic in insulinopenic conditions, suggesting that unopposed glucagon action is... 
Diabetes | Glucagon | Tamoxifen | Insulin | GCGR | GLP-1R | MAMMALIAN TARGET | RAT-LIVER | RAPAMYCIN | ALPHA-CELL HYPERPLASIA | BLOOD-GLUCOSE | KNOCKOUT MICE | DISRUPTION | DEFICIENT | ENDOCRINOLOGY & METABOLISM | GROWTH-FACTOR
Journal Article
Biochemical Pharmacology, ISSN 0006-2952, 10/2016, Volume 118, pp. 68 - 87
Class B GPCRs can activate multiple signalling effectors with the potential to exhibit biased agonism in response to ligand stimulation. Previously, we... 
G protein-coupled receptor | Cell signaling | Biased agonism | Glucagon-like peptide-1 receptor | 3RD INTRACELLULAR LOOP | 2ND EXTRACELLULAR LOOP | CRITICAL DETERMINANTS | AGONIST BINDING | VPAC RECEPTOR | PROTEIN-COUPLED RECEPTOR | ADENYLYL-CYCLASE | PARATHYROID-HORMONE | PHARMACOLOGY & PHARMACY | GLP-1 RECEPTOR | BETA-ADRENERGIC RECEPTOR | Cricetulus | Humans | Glucagon-Like Peptide-1 Receptor - chemistry | Glucagon-Like Peptide-1 Receptor - genetics | Glucagon-Like Peptide-1 Receptor - metabolism | Conserved Sequence | Protein Interaction Domains and Motifs | Protein Stability | Radioligand Assay | Binding Sites | CHO Cells | Recombinant Proteins - metabolism | Mutagenesis, Site-Directed | Signal Transduction | Models, Molecular | Recombinant Proteins - chemistry | Mutant Proteins - metabolism | Amino Acid Motifs | Animals | Hydrogen Bonding | Mutant Proteins - chemistry | Ligands | Molecular Docking Simulation | Structural Homology, Protein | Kinetics | Glucagon-Like Peptide-1 Receptor - agonists | Amino Acid Substitution | Glucagon | Index Medicus | CHO, Chinese hamster ovary | GCGR, glucagon receptor | FBS, fetal bovine serum | cAMP, 3′,5′-cyclic adenosine monophosphate | PBS, phosphate buffered saline | iCa2+, intracellular calcium | GPCR, G protein-coupled receptor | TM, transmembrane helix | GLP-1, glucagon-like peptide-1 | DMEM, Dulbecco’s modified Eagle medium | CRF1R, corticotrophin releasing factor receptor-1 | pERK, extracellular signal-regulated kinase 1 and 2 phosphorylation
Journal Article
Journal of Reproductive Immunology, ISSN 0165-0378, 2010, Volume 86, Issue 2, pp. 110 - 111
Journal Article
Journal of clinical pharmacology, ISSN 0091-2700, 2015, Volume 55, Issue 3, pp. 298 - 306
Journal Article
Molecular Genetics and Metabolism Reports, ISSN 2214-4269, 12/2018, Volume 17, pp. 46 - 52
Glucagon receptor (GCGR) defect (Mahvash disease) is an autosomal recessive hereditary pancreatic neuroendocrine tumor (PNET) syndrome that has only been... 
Pancreatic α cell hyperplasia (ACH) | Glucagon receptor | Pancreatic neuroendocrine tumor (PNET) | Newborn screening | GCGR mutation | Mahvash disease | Hyperaminoacidemia | HYPERGLUCAGONEMIA | INHIBITION | Pancreatic alpha cell hyperplasia (ACH) | ALPHA CELL HYPERPLASIA | GENETICS & HEREDITY
Journal Article
Diabetes, Obesity and Metabolism, ISSN 1462-8902, 02/2018, Volume 20, Issue 2, pp. 283 - 291
AimsGlucagon receptor (GCGR) blockers are being investigated as potential therapeutics for type 1 and type 2 diabetes. Here we report the safety, tolerability,... 
phase 1 | glucagon stimulation | REGN | 1193 | GCGR | REGN1193 | ALPHA-CELLS | BLOOD-GLUCOSE | PANCREAS | HYPERPLASIA | ANTAGONIST LY2409021 | ISLET-CELL TUMOR | INSULIN | ENDOCRINOLOGY & METABOLISM | MICE | SECRETION | TYPE-2 DIABETES-MELLITUS | Receptors, Glucagon - antagonists & inhibitors | Follow-Up Studies | Humans | Middle Aged | Antibodies, Monoclonal - adverse effects | Half-Life | Male | Metabolic Clearance Rate | Antibodies, Blocking - pharmacology | Patient Dropouts | Antibodies, Blocking - administration & dosage | Dose-Response Relationship, Drug | Young Adult | Hypoglycemic Agents - administration & dosage | Adult | Female | Antibodies, Blocking - blood | Hypoglycemic Agents - pharmacokinetics | Lost to Follow-Up | Blood Glucose - analysis | Double-Blind Method | Antibodies, Monoclonal - pharmacology | Antibodies, Monoclonal - pharmacokinetics | Receptors, Glucagon - metabolism | Biomarkers - blood | Hypoglycemic Agents - pharmacology | Antibodies, Blocking - adverse effects | Antibodies, Monoclonal - administration & dosage | Infusions, Intravenous | Hypoglycemic Agents - adverse effects | Cohort Studies | Type 2 diabetes | Hyperglycemia | Safety and security measures | Glucagon | Analysis | Therapeutics | Monoclonal antibodies | Glucose | Dextrose | Homeopathy | Materia medica and therapeutics | Food | Lipoproteins (low density) | Pharmacodynamics | Diabetes mellitus | Liver | Diabetes mellitus (insulin dependent) | Hypoglycemia | Plasma levels | Safety | Pharmacokinetics | Diabetes mellitus (non-insulin dependent) | Nonlinear systems | Index Medicus | Original
Journal Article
Molecular Metabolism, ISSN 2212-8778, 2016, Volume 5, Issue 8, pp. 731 - 736
Abstract Objective It has been thought that the depletion of insulin is responsible for the catabolic consequences of diabetes; however, evidence suggests that... 
Endocrinology & Metabolism | Glucose metabolism | Mice | Lipid metabolism | Glucagon | Type 1 diabetes | Insulin | HYPERGLUCAGONEMIA | DISRUPTION | ENDOCRINOLOGY & METABOLISM
Journal Article
Molecular Metabolism, ISSN 2212-8778, 04/2019, Volume 22, pp. 37 - 48
Administration of glucagon (GCG) or GCG-containing co-agonists reduces body weight and increases energy expenditure. These actions appear to be transduced by... 
Energy expenditure | Thermogenesis | Glucagon | brown adipose tissue | Adiposity | Lipolysis | STIMULATION | ADIPOCYTES | CATECHOLAMINES | INSULIN | GROWTH | ENDOCRINOLOGY & METABOLISM | NORADRENALINE | METABOLIC-RATE | MODULATION | AGONIST
Journal Article