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游离脂肪酸(FFAs)是一种重要能量来源并起到信号分子的作用,外周游离脂肪酸水平升高与糖尿病、肥胖以及脂代谢紊乱紧密相关.G蛋白偶联受体(G protein-coupled re-ceptors,GPCR)是一种含有7个α螺旋的整合膜蛋白,是细胞表面最大的受体超家族.GPR120是一种新发现的游离脂肪酸受体,它直接或者间接参与调节体内一系列代谢过程,如激素分泌、葡萄糖代谢、脂质生成、信号转导等.作为一潜在的治疗多种代谢疾病的药物靶标,GPR120的生理功能及作用的分子机制等都值得进一步研究. 相似文献
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游离脂肪酸(FFAs)是一种重要能量来源并起到信号分子的作用,外周游离脂肪酸水平升高与糖尿病、肥胖以及脂代谢紊乱紧密相关。G蛋白偶联受体(G protein-coupled re-ceptors,GPCR)是一种含有7个α螺旋的整合膜蛋白,是细胞表面最大的受体超家族。GPR120是一种新发现的游离脂肪酸受体,它直接或者间接参与调节体内一系列代谢过程,如激素分泌、葡萄糖代谢、脂质生成、信号转导等。作为一潜在的治疗多种代谢疾病的药物靶标,GPR120的生理功能及作用的分子机制等都值得进一步研究。 相似文献
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Pradeep Paudel Su Hui Seong Se Eun Park Jong Hoon Ryu Hyun Ah Jung Jae Sue Choi 《Marine drugs》2021,19(6)
Phlorotannins are polyphenolic compounds in marine alga, especially the brown algae. Among numerous phlorotannins, dieckol and phlorofucofuroeckol-A (PFF-A) are the major ones and despite a wider biological activity profile, knowledge of the G protein-coupled receptor (GPCR) targets of these phlorotannins is lacking. This study explores prime GPCR targets of the two phlorotannins. In silico proteocheminformatics modeling predicted twenty major protein targets and in vitro functional assays showed a good agonist effect at the α2C adrenergic receptor (α2CAR) and an antagonist effect at the adenosine 2A receptor (A2AR), δ-opioid receptor (δ-OPR), glucagon-like peptide-1 receptor (GLP-1R), and 5-hydroxytryptamine 1A receptor (5-TH1AR) of both phlorotannins. Besides, dieckol showed an antagonist effect at the vasopressin 1A receptor (V1AR) and PFF-A showed a promising agonist effect at the cannabinoid 1 receptor and an antagonist effect at V1AR. In silico molecular docking simulation enabled us to investigate and identify distinct binding features of these phlorotannins to the target proteins. The docking results suggested that dieckol and PFF-A bind to the crystal structures of the proteins with good affinity involving key interacting amino acid residues comparable to reference ligands. Overall, the present study suggests α2CAR, A2AR, δ-OPR, GLP-1R, 5-TH1AR, CB1R, and V1AR as prime receptor targets of dieckol and PFF-A. 相似文献
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