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anti-Human Glucagon Receptor Antikörper:
anti-Mouse (Murine) Glucagon Receptor Antikörper:
anti-Rat (Rattus) Glucagon Receptor Antikörper:
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Human Polyclonal Glucagon Receptor Primary Antibody für IHC (p) - ABIN271047
Mighiu, Yue, Filippi, Abraham, Chari, Lam, Yang, Christian, Charron, Lam: Hypothalamic glucagon signaling inhibits hepatic glucose production. in Nature medicine 2013
Show all 2 Pubmed References
Human Polyclonal Glucagon Receptor Primary Antibody für IF (p), IHC (p) - ABIN751528
Rafacho, Gonçalves-Neto, Santos-Silva, Alonso-Magdalena, Merino, Taboga, Carneiro, Boschero, Nadal, Quesada: Pancreatic alpha-cell dysfunction contributes to the disruption of glucose homeostasis and compensatory insulin hypersecretion in glucocorticoid-treated rats. in PLoS ONE 2014
Human Polyclonal Glucagon Receptor Primary Antibody für ELISA - ABIN314296
Sørensen, Winzell, Brand, Fosgerau, Gelling, Nishimura, Ahren: Glucagon receptor knockout mice display increased insulin sensitivity and impaired beta-cell function. in Diabetes 2006
Human Polyclonal Glucagon Receptor Primary Antibody für ICC, IF - ABIN4314511
Lenders, Pacak, Huynh, Sharabi, Mannelli, Bratslavsky, Goldstein, Bornstein, Eisenhofer: Low sensitivity of glucagon provocative testing for diagnosis of pheochromocytoma. in The Journal of clinical endocrinology and metabolism 2010
3.0 A-resolution crystal structure of the full-length human glucagon receptor (GCGR) in complex with a glucagon (zeige GCG Antikörper) analogue and partial agonist, NNC1702
work toward the mapping of interactions between the polypeptide hormone glucagon (zeige GCG Antikörper) and the glucagon receptor
3.0 A crystal structure of full-length GCGR containing both the extracellular domain and transmembrane domain in an inactive conformation
This work suggests that RAMP2 (zeige RAMP2 Antikörper) may modify the agonist activity and trafficking of the GCGR, with potential relevance to production of new peptide analogs with selective agonist activities.
Data suggest that GCGR activation proceeds via a mechanism in which transmembrane helix 6 (TM6) is held in an inactive conformation by a conserved polar core and a hydrophobic lock (involving intracellular loop 3, IC3); mutations in the corresponding polar core of GCGR disrupt these inhibitory elements, allow TM6 to swing outward, and induce constitutive G protein signaling.
The activation of the GCGR is characterized by the outward movement of the intracellular side of helix VI. In the active state of the GCGR, the Arg173(2.46)-Ser350(6.41) and Glu245(3.50)-Thr351(6.42) hydrogen bonds break, and the chi1 rotamer of Phe322(5.54) changes from perpendicular to parallel to helix VI.
In the glucagon receptor (GCGR) and glucagon-like peptide-1 receptor (GLP-1R (zeige GLP1R Antikörper)), the extracellular domain is required for signaling even when the hormone is covalently linked to the transmembrane domain.
2.5 A crystal structure of human GCGR in complex with the antagonist MK-0893, which is found to bind to an allosteric site outside the seven transmembrane helical bundle in a position between TM6 and TM7 extending into the lipid bilayer
Molecular dynamics and disulfide crosslinking studies suggest that apo (zeige C9orf3 Antikörper)-GCGR can adopt both an open and closed conformation associated with extensive contacts between the ECD (zeige SHFM1 Antikörper) and 7TM domain. Glucagon (zeige GCG Antikörper) binds to GCGR by a conformational selection mechanism.
glucagon (zeige GCG Antikörper) cell adenomatosis with GCGR germline mutations seems to follow an autosomal-recessive trait.
we show that glucagon receptor (GCGR) inhibition with a monoclonal antibody normalized blood glucose and beta-hydroxybutyrate levels. Insulin receptor (zeige INSR Antikörper) antagonism increased pancreatic beta-cell mass threefold. Normalization of blood glucose levels with GCGR-blocking antibody unexpectedly doubled beta-cell mass relative to that observed with S961 alone and 5.8-fold over control
These results show that Slc38a5 (zeige Slc38a5 Antikörper) is a key component of the feedback circuit between glucagon receptor signaling in the liver and amino-acid-dependent regulation of pancreatic alpha cell mass in mice.
GcgR knockout (Gcgr(-/-)) mice displayed lower blood glucose levels accompanied by elevated plasma ghrelin (zeige GHRL Antikörper) levels. Hyperglycemia was averted in streptozocin treated Gcgr(-/-) mice and the plasma ghrelin (zeige GHRL Antikörper) level was further increased.
glucagon receptor antagonist improves glycemia in diet-induced obese angptl4 (zeige ANGPTL4 Antikörper) knockout mice without increasing glucagon (zeige GCG Antikörper) levels or alpha-cell proliferation, underscoring the importance of this protein.
Data indicate that the exocrine pancreas in the glucagon receptor Gcgr-/- mice exhibited larger nuclear size than in WT or heterozygous controls, most obviously at old ages.
Simultaneous and sufficient activation of GLP1R (zeige GLP1R Antikörper) is required to reduce GCCR (zeige NR3C1 Antikörper) mediated blood glucose elevation following administration of a GLP1R (zeige GLP1R Antikörper)/GCGR co-agonist.
Knockdown of liver glucagon receptor in mice reduces blood glucose and increases blood LDL levels.
Gcgr(-/-) mice became lethargic (zeige CACNB4 Antikörper) & cachexic & died early. Autopsy revealed numerous PNETs up to 15 mm in diameter in most well-preserved Gcgr(-/-) pancreata.
Data suggest that GcgR activation raises hepatic expression of fibroblast growth factor 21 (FGF21 (zeige FGF21 Antikörper)) and increases circulating levels of FGF21 (zeige FGF21 Antikörper); GcgR activation induces body weight loss and stimulates lipid metabolism.
These results suggest that a circulating factor generated after disruption of hepatic Gcgr signaling can increase alpha-cell proliferation independent of direct pancreatic input.
The protein encoded by this gene is a glucagon receptor that is important in controlling blood glucose levels. Defects in this gene are a cause of non-insulin-dependent diabetes mellitus (NIDDM).
, glucagon receptor-like
, glucagon receptor perhaps same as Niddm3