ライフサイエンスコーパス: GLP1R

1 GLP1R is highly expressed on pancreatic beta-cells, and

2 Importantly, as a GLP1R interactor, ATP6ap2 was required for GLP1-induced

3 LP1R bound to the peptide Exendin-4 (Exe4; a GLP1R agonist on the market for treating diabetes) using

4 that are distinct from those obtained with a GLP1R-selective agonist.

5 We examined whether a long acting GLP1R/GCGR dual agonist peptide exerts metabolic effects

6 then administered liraglutide, a long-acting GLP1R agonist.

7 body weight-lowering effects of long-acting GLP1R agonists are via direct action on CNS GLP1R or the

8 ver, their function is dependent on adequate GLP1R expression, which is downregulated in diabetes.

9 it also enhanced islet GLP1R expression and GLP1R agonist-induced insulin secretion and glucose tole

10 vel dual role in beta cells, modulating both GLP1R signaling and insulin processing to affect insulin

11 effects of DualAG require activation of both GLP1R and GCGR.

12 and ATP6ap2 were co-expressed in beta cells, GLP1R was shown to directly interact with ATP6ap2, as as

13 GLP1R agonists are via direct action on CNS GLP1R or the result of downstream activation of afferent

14 1R/GCGR agonist, DualAG, and a corresponding GLP1R-selective agonist, GLPAG, matched for GLP1R agonis

15 N AND We developed a protease-resistant dual GLP1R/GCGR agonist, DualAG, and a corresponding GLP1R-se

16 GLP1R-selective agonist, GLPAG, matched for GLP1R agonist potency and pharmacokinetics.

17 enes involved in plasma glucose homeostasis (GLP1R) and lipid metabolism as well as maternal-fetal li

18 However, GLP1R is a member of the class B1 family of GPCRs for wh

19 tion of a low-frequency nonsynonymous SNV in GLP1R (A316T; rs10305492; MAF=1.4%) with lower FG (beta=

20 cal distension of the stomach and intestine (GLP1R neurons).

21 Indeed, it also enhanced islet GLP1R expression and GLP1R agonist-induced insulin secre

22 , in vivo deletion of miR-204 promoted islet GLP1R expression and enhanced responsiveness to GLP1R ag

23 in both chow- and high-fat-fed mice lacking GLP1R in the CNS or visceral nerves; however, liraglutid

24 f downstream activation of afferent neuronal GLP1R.

25 oned taste aversion in mice lacking neuronal GLP1R.

26 These data indicate that neuronal GLP1Rs mediate body weight and anorectic effects of lira

27 in yeast two-hybrid assays to identify novel GLP1R interactors in both mouse and human islets.

28 ng ligand binding and receptor activation of GLP1R and other class B1 GPCRs.

29 e enabled delineation of the contribution of GLP1R versus GCGR activation to the pharmacology of Dual

30 objective was to use a method independent of GLP1R antibodies to identify and characterize the target

31 We found that neither reduction of GLP1R in the CNS nor in the visceral nerves resulted in

32 d the transmembrane (TM) bundle structure of GLP1R bound to the peptide Exendin-4 (Exe4; a GLP1R agon

33 The activation and transduction of GLP1R requires complex interactions with a host of acces

34 RNA, miR-204, directly targets the 3' UTR of GLP1R and thereby downregulates its expression in the be

35 ls, and activation by endogenous incretin or GLP1R agonists increases cAMP generation, which stimulat

36 Glucagon-like peptide 1 receptor (GLP1R) agonists are widely used to treat diabetes.

37 The glucagon-like peptide 1 receptor (GLP1R) is a G protein-coupled receptor (GPCR) involved i

38 ng which tissues express the GLP-1 receptor (GLP1R) is critical for the development of GLP-1-based th

39 a glucagon-like peptide 1 (GLP-1) receptor (GLP1R)/glucagon receptor (GCGR) dual agonist peptide tha

40 GLP1 activates its receptor, GLP1R, to enhance insulin secretion.

41 by the brain, which contains GLP1 receptors (GLP1R).

42 Sustained GLP1R/GCGR dual agonism reverses obesity in DIO mice and

43 present studies show for the first time that GLP1R is under the control of a microRNA, miR-204, and u

44 y a group of proteins that interact with the GLP1R.

45 cts of OXM have been attributed primarily to GLP1R agonism.

46 1R expression and enhanced responsiveness to GLP1R agonists, resulting in improved glucose tolerance,

47 When GLP1R and ATP6ap2 were co-expressed in beta cells, GLP1R

48 nd 14 strong polar interactions of Exe4 with GLP1R, of which 8 interactions are in the TM bundle (2 i