anti-G Protein-Coupled Receptor 81 (GPR81) Anticorps

Mouse (Murine) G Protein-Coupled Receptor 81 (GPR81) interaction partners

1. these results demonstrate that lactic-acid-producing bacteria -type symbiont-derived lactate plays a pivotal role in promoting intestinal stem-cell -mediated epithelial development in a Gpr81-dependent manner

2. Manipulation of the GPR81 pathway could provide novel opportunities for enhancing regulatory responses and treating colonic inflammation.

3. Study using Hcar1-KO mice identified the lactate receptor Hcar1 as a key regulator of Vegf and angiogenesis in the brain and as an initial mediator of cerebral effects of physical exercise.

4. lactate can induce GPR81-independent metabolic changes that modulate macrophage pro-inflammatory activation.

5. GPR81 expression increased during gestation, and peaked near labor. GPR81 is expressed in the uterus with high expression in myometrium. GPR81 mediates inflammation in the laboring uterus.

6. Results indicate that lactate may aggravated ischemic brain injury by activating GPR81 and inhibition of GPR81 protects against ischemia-induced cell death via an antiapoptosis pathway

7. Description of a GPR81 selective agonist with in vivo efficacy, inhibiting lipolysis without flushing.

8. Lactate negatively regulates TLR induction of the NLRP3 inflammasome and production of IL1beta, via ARRB2 and GPR81 in liver and pancreatic injury.

9. chronic obesity reduces GPR109A and GPR81 expression in the adipose tissue, while acute in vitro LPS treatment increases expression of GPR109A in adipocytes and macrophages.

10. Inflammation decreases the expression of GPR81 in adipose tissue

11. An autocrine lactate loop mediates insulin-dependent inhibition of lipolysis through GPR81.

12. GPR81 couples to the Gi signaling pathway

13. Data show that siRNA-mediated knockdown of PPARgamma in differentiated 3T3-L1 adipocytes showed a significant decrease in Gpr81 protein expression.

Human G Protein-Coupled Receptor 81 (GPR81) interaction partners

1. The novel role of HCAR1 in development of chemoresistance in cervical carcinoma HeLa cells via ABCB1 transporter up-regulation.

2. Findings identify GPR81 as a tumor-promoting receptor in breast cancer progression and suggest a novel mechanism that regulates GPR81-dependent activation of the PI3K/Akt signaling axis in tumor microenvironment.

3. Activation of GPR81 decreases intracellular cAMP levels and inhibits PKA activity, leading to activation of TAZ and upregulation of PD-L1. This study reveals a critical role for lactate in the immune checkpoint pathway and an unexpected function of TAZ in tumor evasion of the T-cell-mediated immune response.

4. Lactate receptor/HCAR1 expression in cervical carcinoma cells may contribute to the modulation of cellular DNA repair mechanisms.

5. HCA1/3 are necessary for breast cancer cells to balance lipid/fatty acid metabolism.

6. HCAR1 and monocarboxylate transporters activity is required for the L- and D-lactate-mediated enhancement of DNA repair and of HeLa cell survival.

7. Description of a GPR81 selective agonist with in vivo efficacy, inhibiting lipolysis without flushing.

8. Data support that GPR81 is important for cancer cell regulation of lactate transport mechanisms.

9. Lactate negatively regulates TLR induction of the NLRP3 inflammasome and production of IL1beta, via ARRB2 and GPR81 in liver and pancreatic injury.

10. demonstrated that the C165-E166-S167-F168 motif at the second extracellular loop is critical for GPR81 function, and the conserved six Cys residues at the extracellular regions are necessary for GPR81 function

11. GPR81 with relatively restricted expression in the adipose tissues functions as a receptor for lactate and can mediate an anti-lipolytic effect of lactate.

12. Data show that the coordinated PPARgamma-mediated regulation of the GPR81, GPR109A and GPR109B presents a novel mechanism by which TZDs may reduce circulating free fatty acid levels and perhaps ameliorate insulin resistance in obese patients.