|
1）Ahren B. Islet G protein-coupled receptors as potential targets for treatment of type 2 diabetes. Nat Rev Drug Discov. 2009; 8: 369-85
|
|
|
|
2）Amisten S, Salehi A, Rorsman P, et al. An atlas and functional analysis of G-protein coupled receptors in human islets of Langerhans. Pharmacol Ther. 2013; 139: 359-91
|
|
|
|
|
|
3）Drucker DJ. The biology of incretin hormones. Cell Metab. 2006; 3: 153-65
|
|
|
|
|
|
4）Seino Y, Yabe D. Glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1: Incretin actions beyond the pancreas. J Diabetes Investig. 2013; 4: 108-30
|
|
|
|
|
|
5）Zhang CL, Katoh M, Shibasaki T, et al. The cAMP sensor Epac2 is a direct target of antidiabetic sulfonylurea drugs. Science. 2009; 325: 607-10
|
|
|
|
|
|
6）Seino S, Shibasaki T. PKA-dependent and PKA-independent pathways for cAMP-regulated exocytosis. Physiol Rev. 2005; 85: 1303-42
|
|
|
|
|
|
7）Shibasaki T, Takahashi T, Takahashi H, et al. Cooperation between cAMP signalling and sulfonylurea in insulin secretion. Diabetes Obes Metab. 2014; 16 Suppl 1: 118-25
|
|
|
|
|
|
8）Song WJ, Seshadri M, Ashraf U, et al. Snapin mediates incretin action and augments glucose-dependent insulin secretion. Cell Metab. 2011; 13: 308-19
|
|
|
|
|
|
9）Brozzi F, Lajus S, Diraison F, et al. MyRIP interaction with MyoVa on secretory granules is controlled by the cAMP-PKA pathway. Mol Biol Cell. 2012; 23: 4444-55
|
|
|
|
|
|
10）Kaihara KA, Dickson LM, Jacobson DA, et al. beta-Cell-specific protein kinase A activation enhances the efficiency of glucose control by increasing acute-phase insulin secretion. Diabetes. 2013; 62: 1527-36
|
|
|
|
|
|
11）Kawasaki H, Springett GM, Mochizuki N, et al. A family of cAMP-binding proteins that directly activate Rap1. Science. 1998; 282: 2275-9
|
|
|
|
|
|
12）de Rooij J, Zwartkruis FJ, Verheijen MH, et al. Epac is a Rap1 guanine-nucleotide-exchange factor directly activated by cyclic AMP. Nature. 1998; 396: 474-7
|
|
|
|
|
|
13）Ueno H, Shibasaki T, Iwanaga T, et al. Characterization of the gene EPAC2: structure, chromosomal localization, tissue expression, and identification of the liver-specific isoform. Genomics. 2001; 78: 91-8
|
|
|
|
|
|
14）Niimura M, Miki T, Shibasaki T, et al. Critical role of the N-terminal cyclic AMP-binding domain of Epac2 in its subcellular localization and function. J Cell Physiol. 2009; 219: 652-8
|
|
|
|
|
|
15）Ozaki N, Shibasaki T, Kashima Y, et al. cAMP-GEFII is a direct target of cAMP in regulated exocytosis. Nat Cell Biol. 2000; 2: 805-11
|
|
|
|
|
|
16）Shibasaki T, Takahashi H, Miki T, et al. Essential role of Epac2/Rap1 signaling in regulation of insulin granule dynamics by cAMP. Proc Natl Acad Sci U S A. 2007; 104: 19333-8
|
|
|
|
|
|
17）Yasuda T, Shibasaki T, Minami K, et al. Rim2alpha determines docking and priming states in insulin granule exocytosis. Cell Metab. 2010; 12: 117-29
|
|
|
|
|
|
18）Leech CA, Dzhura I, Chepurny OG, et al. Molecular physiology of glucagon-like peptide-1 insulin secretagogue action in pancreatic beta cells. Prog Biophys Mol Biol. 2011; 107: 236-47
|
|
|
|
|
|
19）Song WJ, Mondal P, Li Y, et al. Pancreatic beta-cell response to increased metabolic demand and to pharmacologic secretagogues requires EPAC2A. Diabetes. 2013; 62: 2796-807
|
|
|
|
|
|
20）Takahashi T, Shibasaki T, Takahashi H, et al. Antidiabetic sulfonylureas and cAMP cooperatively activate Epac2A. Sci Signal. 2013; 6: ra94
|
|
|
|
|
|
21）Gutniak MK, Juntti-Berggren L, Hellstrom PM, et al. Glucagon-like peptide I enhances the insulinotropic effect of glibenclamide in NIDDM patients and in the perfused rat pancreas. Diabetes Care. 1996; 19: 857-63
|
|
|
|
|
|
22）Aaboe K, Knop FK, Vilsboll T, et al. KATP channel closure ameliorates the impaired insulinotropic effect of glucose-dependent insulinotropic polypeptide in patients with type 2 diabetes. J Clin Endocrinol Metab. 2009; 94: 603-8
|
|
|
|
|
|
23）Yabe D, Seino Y. Dipeptidyl peptidase-4 inhibitors and sulfonylureas for type 2 diabetes: Friend or Foe? J Diabetes Investig. 2014; 10.1111/jdi. 12229
|
|
|
|
|
|
24）Mukai E, Fujimoto S, Sato H, et al. Exendin-4 suppresses SRC activation and reactive oxygen species production in diabetic Goto-Kakizaki rat islets in an Epac-dependent manner. Diabetes. 2011; 60: 218-26
|
|
|
|
|