TGR5 (298_330) (Human) _ 100ug
- Known as:
- TGR5 (298_330) (Human) _ 100ug
- Catalog number:
- 002-06
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Phoenix Peptide
- Gene target:
- TGR5 (298_330) (Human) _ 100ug
Related genes to: TGR5 (298_330) (Human) _ 100ug
- Gene:
- GPBAR1 NIH gene
- Name:
- G protein-coupled bile acid receptor 1
- Previous symbol:
- -
- Synonyms:
- BG37, GPCR, TGR5, M-BAR, GPCR19, GPR131, MGC40597
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-24
- Date modifiied:
- 2014-11-19
Related products to: TGR5 (298_330) (Human) _ 100ug
Related articles to: TGR5 (298_330) (Human) _ 100ug
- Metabolic dysfunction-associated steatotic liver disease (MASLD) and cardiovascular-kidney-metabolic (CKM) syndrome are interrelated conditions with shared pathophysiological features; however, the genetic architecture underlying their relationship has not been fully elucidated. Deciphering this shared genetic basis holds promise for advancing mechanistic insights and therapeutic discovery. - Source: PubMed
Publication date: 2026/05/09
Yin KangjiaZhang CaoLiu BingXu RuyunZeng JingEslam MohammedNi Jing - : Based on previous findings on the Lingguizhugan (LGZG)-mediated gut-liver axis, this study clarifies the therapeutic mechanisms of LGZG in metabolic dysfunction-associated steatotic liver disease (MASLD), with a focus on the gut microbiota-bile acid-TGR5 (GPBAR1) axis. : C57BL/6J mice were fed a high-fat diet (HFD) for 8 weeks to induce MASLD, followed by 4-week LGZG intervention (21.57 g/kg/day, oral gavage). Metabolic phenotypes, gut microbiota (16S rRNA sequencing), serum/hepatic bile acids (targeted metabolomics), and molecular targets (qPCR/Western blot) were analyzed. : LGZG significantly alleviated HFD-induced obesity, insulin resistance, and hepatic steatosis, while enhancing whole-body energy expenditure (increased oxygen consumption (VO), and heat production ( < 0.05). It also reduced serum ALT ( < 0.001) and AST levels ( < 0.01). Mechanistically, LGZG remodeled the gut microbiota, specifically increasing , and _NK4A236_group while decreasing . This shift inhibited the intestinal FXR-Fgf15 axis, concurrently activating the hepatic alternative bile acid synthesis pathway (upregulating CYP27A1 and CYP7B1 protein expression; < 0.001 and < 0.01, respectively). Consequently, systemic accumulation of non-12α-hydroxylated bile acids (non-12-OH BAs) such as hyocholic acid (HCA) and 7-ketolithocholic acid (7-ketoLCA) occurred-known TGR5 agonists and intestinal FXR antagonists. These changes elevated serum GLP-1 levels ( < 0.05) and activated adipose TGR5-cAMP/PKA/CREB signaling. The metabolic benefits primarily originated from non-12-OH BAs enrichment and TGR5-mediated adipose browning, not hepatic FXR activation. : Our findings show that LGZG ameliorates MASLD by remodeling bile acid profiles via intestinal FXR-Fgf15 axis inhibition and hepatic alternative synthesis pathway activation. This study highlights the TGR5-targeting properties of LGZG, providing a mechanistic basis for its therapeutic use in metabolic disorders. - Source: PubMed
Publication date: 2026/03/24
Sun Yun-HongDing Pei-LunWang XueWang Yi-RongZhu Ming-ZheWang KaiDai LiangDang Yan-QiJi GuangLi MengZhou Wen-Jun - Hepatic ischemia-reperfusion injury (IRI) is an important factor affecting the prognosis of liver transplantation patients. The role of Arrb2 in liver injury is unclear. Our study aimed to determine the role of Arrb2 in hepatic IRI and to identify its underlying mechanisms. - Source: PubMed
Publication date: 2026/04/24
Wang Xiao-WenZheng Wen-JieChen Hao-QiHuang TaoZhang YuanYan Xi-JingLi Wen-ChaoZou LongWu Jie-ZhongZhu Wen-FengYang Qi-WeiWang Gen-ShuHu Kun-Peng - The presence of an unbalanced gut microbiome and the dysregulation of bile acid signalling are considered pivotal causes of various inflammation-based diseases. The Takeda G protein-coupled receptor (TGR5), TGR5 is a bile acid-responsive receptor that modulates inflammatory signalling pathways, making it an enticing molecular target for the discovery of novel anti-inflammatory agents. Herein, a comprehensive in silico approach was employed to identify potential TGR5 agonists from sterol-rich phytocompounds present in Triphala, a traditional polyherbal formulation. Using in silico computational methods, such as molecular docking and molecular dynamics simulations (MDS), we screened the putative agonistic potential of 10 phytocompounds obtained from , , and against the crystal structure of human TGR5 (PDB ID: 7XTQ). Based on binding energy and molecular interactions, ergosterol (-12.34 ± 0.17 kcal/mol) and stigmasterol (-10.35 ± 0.04 kcal/mol) were predicted to be the top and best compounds. Furthermore, the stability of these two compounds in the docked complex was analysed using MDS for 200 ns. The mean Cα RMSD values were 0.22 ± 0.02 nm for both ergosterol- and stigmasterol-bound complexes, compared to 0.21 ± 0.02 nm for the unbound apo protein. Further, the molecular mechanics/Poisson-Boltzmann surface area (MMPBSA) analysis revealed that ergosterol exhibited binding free energy (-139.868 ± 12.318 kJ/mol) comparable to that of the co-crystallised ligand R399 -93.424 ± 8.919 kJ/mol. In silico ADMET predictions indicated acceptable drug-like properties and low toxicity for both compounds. Collectively, these computational findings suggest that ergosterol is a promising putative TGR5 agonist, warranting further experimental validation of its potential role in modulating inflammation-related pathways. - Source: PubMed
Publication date: 2026/03/30
Prasad Yathindra MaruthiGowda Sneha RamaiahShantamurthy NanditaSehar Allwin Ebinesar Jacob SamuelRazack Sirajunnisa AbdulSrichairatanakool SomdetRavikumar Yuvaraj - Agonists of the G protein-coupled receptor TGR5 have long been sought-after for their metabolic benefits. Intestinal TGR5 activation induces secretion of the antidiabetic hormone GLP-1, which can systemically improve diabetes phenotypes in multiple organs. However, no TGR5 agonist drug candidate has succeeded in clinical trials due to their low potency and unwanted side effects. A challenge in the field has been the development of TGR5 agonists that are non-toxic, long-acting, and have functional selectivity for G protein-biased agonism. In this study, we propose a systematic pipeline for engineering optimal TGR5 agonists with antidiabetic properties. This pipeline is interdisciplinary, combining in silico, in vitro, and in vivo assays to design and validate drug candidates. We identify 2 lead compounds that outline the necessary beneficial properties for a successful TGR5 agonist against diabetes. We uncover the molecular mechanisms that allow TGR5 agonists to induce the transcription of their target, TGR5, in intestinal enteroendocrine cells. Lastly, we investigate the molecular interactions of our lead candidates in the TGR5 binding pocket to identify optimal parameters for stability and biological activity. Our strategy for TGR5 agonist design and evaluation has the potential to guide the discovery process for targeted TGR5 therapeutics for metabolic diseases. - Source: PubMed
Publication date: 2026/03/26
Bhimanwar Rachana SDetwiler ZacharyZhu Jinge GSaghafi Samuel TWinder Carolyn ADavis Dawn BeltMittal AmitSharma VikasHarris David AChaudhari Snehal N