We detected the expression of GPR37 in NSCLC tissues and cell lines. The study explored the influence of GPR37 on tumor cell proliferation. Furthermore, we examined the effects of GPR37 on tumor cell apoptosis and invasion. Most importantly, we investigated whether GPR37 affects cisplatin-induced drug resistance in NSCLC. Knockdown of GPR37 significantly inhibits the occurrence and development of NSCLC.

Efferocytes release extracellular vesicles to resolve inflammation and tissue injury via prosaposin-GPR37 We report that efferocyte-derived EVs express prosaposin, which binds to macrophage GPR37 to increase Neutralization and knockdown of prosaposin or blocking GRP37 abrogates the pro-resolution effects of

contributions to understanding the signaling, regulation and in vivo actions of the neuroprotective receptors GPR37 & GPR37L1 as well as the adhesion GPCRs BAI1, BAI2, and GPR56.

< GPCR News < GPCRs in Oncology and Immunology GPR97 depletion aggravates imiquimod-induced psoriasis In this research, our team allocated GPR97 depletion (GPR97-/-), GPR97 conditional depletion on dendritic cell (DC-cKO), and keratin 14-conditional knockout (K14-cKO) mice models to explore the function of GPR97 It was found that significantly aggravated psoriasis-like lesion in GPR97-/- mice. Particularly, we found that level of NF-κB p65 was increased in GPR97-/- DCs and BDP could inhibit p65

< GPCR News < GPCRs in Oncology and Immunology G protein-coupled estrogen receptor (GPER)/GPR30 forms in MCF7 breast cancer cells Published date January 10, 2024 Abstract "G protein-coupled receptor 30 (GPR30 GPR30 constitutively and PDZ-dependently inhibits β1AR-mediated cAMP production. Deleting the GPR30 C-terminal PDZ motif (-SSAV) does not interfere with the receptor complex, indicating These results argue that GPR30 and β1AR form a PDZ-independent complex in MCF7 cells through which GPR30

The characterized compounds were evaluated on four G-protein coupled receptors (GPCRs: GPR35, muscarinic Molecular docking was conducted on GPR35-active compounds and GPR35 crystal structure. Three compounds showed potent GPR35 agonistic activity (EC50 < 10 μM) and the GPR35 agonism action of Docking results revealed that the GPR35-targeting compounds interacted at the key residues for the agonist-initiated activation of GPR35.

Results: We found that miR-19a, GPR39 mRNA and PKC mRNA were upregulated while GRK6 mRNA was downregulated We further identified that the over-expression of miR-19a could regulate the signaling between GRK6, GPR39 and PKC via the signaling pathway of miR-19a/GRK6/GPR39/PKC, which accordingly resulted in suppressed

Expressed Gpr116 (Adgrf5) Transcript Variants in Mouse Kidney Hailey Steichen Elucidating The Role Of GPR97 Hailey Steichen on the web Zaidman Physiology Lab Elucidating The Role Of GPR97/ADGRG3 In Neutrophil

Recently, we have elucidated the high-resolution structures of GPR97 transitioning from its inactive

Chang Cardiac Research Institute where he investigated the orphan G protein-coupled receptor (GPCR), GPR37L1