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FFAR2 encodes a member of the GP40 family of G protein-coupled receptors that are clustered together on chromosome 19. Additionally we are shipping FFAR2 Antibodies (77) and FFAR2 Kits (4) and many more products for this protein.
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Although both agonist and antagonist ligands contain negatively charged carboxylates that interact with two key positively charged arginine residues in transmembrane domains V and VII (show TH Proteins) of FFA2, there are clear differences in how these interactions occur.
FFAR2 signaling occurs by divergent G protein pathways.
GPR3 agonism potentiates insulin secretion in isolated islets.
GPR43 expression is reduced in monocytes upon siRNA-knockdown of XBP1 (show XBP1 Proteins), while A549 cells overexpressing XBP1 (show XBP1 Proteins) displayed elevated GPR43 levels.
FFAR2 is a potential therapeutic target of T1 diabetes, representing a link between immune response and glucose homeostasis.
FFAR2 is expressed in pancreatic beta cells and mediates an inhibition of insulin (show INS Proteins) secretion by coupling to Gi-type G proteins.
[review] In vivo and in vitro studies suggest that short-chain fatty acid receptors (SCFAs) stimulate gut (show GUSB Proteins) hormone secretion; therefore, the SCFA-FFA signal is likely to be important for gut (show GUSB Proteins) physiological functions.
GPR43 modulates NF-kappaB (show NFKB1 Proteins) activity via beta-arrestin 2 (show ARRB2 Proteins).
Propionate-stimulated GPR41 (show FFAR3 Proteins) strongly coupled to ERK1/2 activation, while the coupling of linoleic acid-activated GPR40 and acetate-activated GPR43 was weaker.
Selective orthosteric free fatty acid receptor 2 (FFA2) agonists: identification of the structural and chemical requirements for selective activation of FFA2 versus FFA3.
Data (including data from studies in knockout mice) suggest Ffar2 expression in pancreatic beta-cells plays role in gestational glucose homeostasis; this mechanism involves gut microbiome (which contributes to plasma short-chain fatty acid levels).
High fat diet fed GPR43 KO mice develop glucose intolerance due to a defect in insulin (show INS Proteins) secretion, reduced beta-cell mass and expression of differentiation genes. GPR3 (show GPR3 Proteins) agonism potentiates insulin (show INS Proteins) secretion.
GPR-43-deficient mice show a greatly decreased inflammatory reaction to knee injection of monosodium urate crystals in a mouse model of gout.
These findings establish GPR43 as a sensor for excessive dietary energy, thereby controlling body energy utilization while maintaining metabolic homoeostasis.
Data from transgenic mice suggest that Ffar2/Gpr43 and Ffar3/Gpr41 (show FFAR3 Proteins) both act as sensors for short-chain fatty acids in enteroendocrine cells; Ffar2/Gpr43 appears to play this role alone in enteric leukocytes and Ffar3/Gpr41 (show FFAR3 Proteins) alone in enteric neurons.
Short-chain fatty acids activate GPR43 and on intestinal epithelial cells, leading to mitogen-activated protein kinase (show MAPK1 Proteins) signaling and rapid production of chemokines and cytokines. These pathways mediate protective immunity and tissue inflammation in mice.
Data suggest that alpha-gustducin (show GNAT3 Proteins) in colonic mucosa is a key signaling molecule coupling free fatty acid receptors (Gpr43, Gpr119 (show GPR119 Proteins), Gpr120) and possibly bile acid receptor (show NR1H4 Proteins) (TGR5 (show GPBAR1 Proteins)) to secretion of GLP-1 (glucagon-like peptide 1 (show GCG Proteins)).
Inulin-type fructans, paradoxically counteract GPR43 overexpression induced in the adipose tissue by an high fat diet.
This gene encodes a member of the GP40 family of G protein-coupled receptors that are clustered together on chromosome 19. The encoded protein is a receptor for short chain free fatty acids and may be involved in the inflammatory response and in regulating lipid plasma levels.
G protein-coupled receptor 43
, G-protein coupled receptor 43
, free fatty acid activated receptor 2
, leukocyte-specific STAT-induced GPCR