Use your antibodies-online credentials, if available.
抗Human GLP1R 抗体:
抗Mouse (Murine) GLP1R 抗体:
抗Rat (Rattus) GLP1R 抗体:
Human Polyclonal GLP1R Primary Antibody for DB, ICC - ABIN4314326
Kedees, Guz, Grigoryan, Teitelman: Functional activity of murine intestinal mucosal cells is regulated by the glucagon-like peptide-1 receptor. in Peptides 2013
Show all 7 Pubmed References
Human Polyclonal GLP1R Primary Antibody for IHC, IHC (p) - ABIN270557
Matveyenko, Dry, Cox, Moshtaghian, Gurlo, Galasso, Butler, Butler: Beneficial endocrine but adverse exocrine effects of sitagliptin in the human islet amyloid polypeptide transgenic rat model of type 2 diabetes: interactions with metformin. in Diabetes 2009
Show all 3 Pubmed References
Human Polyclonal GLP1R Primary Antibody for IF (p), IHC (p) - ABIN731333
Zhou, Yang, Xin, Li, Guo, Hu, Zhou, Zhang, Zhang, Han, Chen: Exendin-4 protects adipose-derived mesenchymal stem cells from apoptosis induced by hydrogen peroxide through the PI3K/Akt-Sfrp2 pathways. in Free radical biology & medicine 2014
Show all 2 Pubmed References
Human Monoclonal GLP1R Primary Antibody for CyTOF, FACS - ABIN4899829
Thompson, Stephens, Bain, Kanamarlapudi: Molecular Characterisation of Small Molecule Agonists Effect on the Human Glucagon Like Peptide-1 Receptor Internalisation. in PLoS ONE 2016
Role of cysteine 341 and arginine 348 of GLP-1 receptor in G-protein coupling.
cryo-electron microscopy structure of the peptide-activated GLP-1R-Gs complex at near atomic resolution
cryo-EM structure of the human GLP-1 receptor in complex with the G protein-biased peptide exendin-P5 and a Galphas (显示 GNAS 抗体) heterotrimer, determined at a global resolution of 3.3 A
The results demonstrate the exendin-4 induces a partial reduction in triglycerides in steatotic hepatocytes within 12 h via the GLP-1 receptor-mediated activation of protein kinase A. Thus, the reduction in hepatocyte triglyceride accumulation is likely driven primarily by downregulation of lipogenesis and upregulation of beta-oxidation of free fatty acids
Data (including data from studies in knockout mice) suggest that MIR204 (which is highly enriched in beta-cells) directly targets 3'-untranslated region of GLP1R and thereby down-regulates expression of GLP1R in beta-cells. Studies were also conducted in primary human and mouse beta-cells and in rat insulinoma (显示 RPS15 抗体) cell line.
Data suggest that GLP1R signaling in pancreatic beta-cells leading to insulin (显示 INS 抗体) secretion involves interactions of GLP1R with HIP1 (显示 HIP1 抗体), SNX1 (显示 SNX1 抗体), and SNX27 (显示 SNX27 抗体); HIP1 (显示 HIP1 抗体) appears to regulate coupling of cell surface GLP1R activation with endocytosis; SNX1 (显示 SNX1 抗体) and SNX27 (显示 SNX27 抗体) appear to control balance between GLP1R plasma membrane recycling and lysosomal degradation.
The GLP-1R was abundantly expressed in numerous regions, including the septal nucleus, hypothalamus, and brain stem.
This is the first time that human Epicardial adipose tissue is found to express both GLP-1R and GLP-2R (显示 GLP2R 抗体) genes.
Changes in GLP-1 (显示 GCG 抗体) levels are associated with weight loss in newly diagnosed Chinese diabetes patients receiving acarbose
the present study revealed that overexpression of GLP1R significantly reduces proliferation, migration and cytokine release in ASM (显示 SMPD1 抗体) cells from COPD (显示 ARCN1 抗体) patients; this involved a significant increase in ABCA1 (显示 ABCA1 抗体) expression levels. This provided evidence to suggest that GLP1R may be a potential therapeutic target for the treatment of COPD (显示 ARCN1 抗体).
IL-33 (显示 IL33 抗体), GLP-1R, and CCL20 (显示 CCL20 抗体) are deregulated in human inflammatory bowel disease. GLP-1 receptor agonists upregulate IL-33 (显示 IL33 抗体), mucin 5b, and CCL20 (显示 CCL20 抗体) in murine Brunner's glands. GLP-1 receptor agonists affect gut (显示 GUSB 抗体) homeostasis in both proximal and distal parts of the gut (显示 GUSB 抗体).
Data show that exendin-4 (Ex-4) could attenuate breast cancer cell proliferation via activation of glucagonlike peptide-1 (GLP-1) receptor (GLP-1R) and subsequent inhibition of nuclear factor kappaB (NF-kappaB (显示 NFKB1 抗体) ) activation.
Glucagon (显示 GCG 抗体)-like peptide (GLP)-1 (显示 GCG 抗体) modulates epithelial ion transport indirectly by activating calcitonin gene-related peptide (CGRP (显示 CALCA 抗体))-containing submucosal enteric neurons in the mouse colon. This GLP-1 (显示 GCG 抗体)-CGRP (显示 CALCA 抗体) response was area-specific and could potentially contribute to the diarrheal side effect of certain GLP-1 receptor therapeutics.
Data (including data from studies using transgenic and knockout mice) suggest that Glp1 (显示 GCG 抗体)/Glp1r signaling in insulin (显示 INS 抗体)-secreting cells plays important role in development of glucose intolerance in obesity; however, Glp1r is not required in insulin (显示 INS 抗体)-secreting cells for improvement in glucose intolerance after weight loss due to bariatric surgery (here, vertical sleeve gastrectomy).
GLP-1R signaling in paraventricular thalamic nucleus plays a role in food intake control.
GLP-1 receptor agonists suppress the progression of atherosclerosis by inhibiting vascular smooth muscle cell proliferation and enhancing AMP-activated protein kinase (显示 PRKAA2 抗体) and cell cycle regulation in ApoE (显示 APOE 抗体) deficient mice.
findings identify a group of proteins that interact with GLP-1R and show that one specific interacting protein, SERP1 (显示 SERP1 抗体), has an important role in facilitating the glycosylation of GLP-1R and rescuing its activities after ER stress induced by tunicamycin.
Suggest transcription factor 7-like 2 (显示 TCF7L2 抗体) is a possible regulator of glucagon-like peptide 1 receptor expression in endothelial/smooth muscle cells in diabetic mice.
ventromedial hypothalamus GLP-1R regulates food intake by engaging key nutrient sensors but is dispensable for the effects of GLP (显示 GOLGA6A 抗体)-1RA on nutrient homeostasis
GLP-1R is highly expressed within the lateral septum.
Study showe that GLP (显示 GOLGA6A 抗体)-producing fibers interact with hypothalamic arcuate nucleus (ARC (显示 NOL3 抗体)) Kiss1 (显示 KISS1 抗体) cells that express GLP-1R, and GLP-1R signaling directly activates ARC (显示 NOL3 抗体) Kiss1 (显示 KISS1 抗体) function in an estradiol-independent manner. Pharmacological activation of GLP-1R signaling during fasting or pharmacological inhibition of CNS GLP-1R signaling during normal feeding does not alter circulating luteinizing hormone levels.
induces insulin secretion\; mediates neuroendocrine signaling of feeding behavior\; mediates cardiovascular response and increased blood pressure
glucagon-like peptide 1 receptor
, glucagon-like peptide 1 receptor-like
, GLP-1 receptor
, pancreatic beta cell receptor for the gluco-incretin hormone glucagon-like peptide 1