ARRB1 (Arrestin Beta 1)

Furthermore, ARRB1 deficiency conferred protection against myeloma-induced bone disease, suggesting a dual role in immune regulation and bone homeostasis. These findings establish ARRB1 as a critical negative regulator of host anti-myeloma immunity and identify it as a potential therapeutic target for enhancing immunotherapy efficacy in MM.

Additionally, IL-1R1/TLR-activated βarr2K295 deSUMOylation drives TRAF6CCD-βarr2 coupling in Mϕs, and βarr2K295 deSUMOylation in vascular Mϕs promotes OR6A2-mediated atherosclerosis in high-cholesterol-diet-fed Ldlr-/- mice. In conclusion, IL-1R1/TLR-induced TRAF6CCD-βarr2 coupling, by inhibiting βarr2/AP2-mediated OR6A2 endocytosis, promotes atherogenic OR6A2-mediated NLRP3 inflammasome activation in vascular Mϕs.

ARRB1 nuclear translocation enhances CA9 transcriptional activity following simulated space radiation and/or microgravity exposure. In short, changes in intracellular calcium concentration play a crucial role in ARRB1 nuclear translocation and subsequent malignant transformation.

SIGNIFICANCE STATEMENT: A small molecule inverse agonist of the atypical chemokine receptor 3 (ACKR3), named VUF16840, is characterized in this work. It was shown that VUF16840 was able to inhibit basal as well as ligand-induced ACKR3 activation and, moreover, inhibits the scavenging function of ACKR3.

Moreover, CYP4X1 and sEH levels jointly predict prognosis and immune infiltration in human colon cancer. Together, this study highlights that CYP4X1/sEH-dependent endocannabinoid metabolism controls CAF-mediated immune evasion, and targeting the CYP4X1/sEH-14,15-EET-EA-GPR119 axis represents a promising therapeutic strategy for improving anti-PD-1 therapy in colon cancer.

These findings highlight an unappreciated potential for biased signaling in the pharmacology of GPR17 ligands. We anticipate that these insights will help to inform the translation of GPR17-targeted therapies and improve our understanding of GPR17-mediated signaling pathways in governing myelination.

Moreover, the combination of Endothall and Cisplatin is high synergistic in treating OS. In conclusion, the study elucidates the pro-oncogenic role of lactate-activated HCAR1 in OS.

Despite earlier evidence of 5-HT2C G protein coupling promiscuity, the full signaling landscape remains incompletely characterized, which may help explain the limited efficacy and potential cancer risks associated with lorcaserin...Profiling of both 5-HT2C-selective and psychedelic ligands reveals diverse signaling profiles, with serotonergic psychedelics such as LSD and psilocin exhibiting a striking Gq/11 bias due to minimal secondary G protein activation. Altogether, this work provides a foundation for incorporating a broader view of 5-HT2C signaling modalities into future investigations of 5-HT2C drug development efforts.

Thus, our results indicate that ATG7 expression in fibroblasts plays a vital role in regulating breast cancer tumorigenesis and progression by modifying stromal-epithelial crosstalk and remodeling the tumor microenvironment (TME). These results suggest that ATG7 can function as a tumor suppressor and represent a new candidate for prognosis and targeted therapy.

Additionally, LcrV treatment reprograms tumor cells by reducing stemness-associated proteins OCT4 and c-MYC. Our findings highlight the potential of biased GPCR agonists as a novel GPCR-targeting strategy for cancer treatment.

Furthermore, we demonstrate that 2-DG effectively inhibits the malignancy-promoting capabilities of ARRB1-Δexon13 by reducing pyruvate levels. Our identification of alternative RNA splicing events of ARRB1 reveals a mechanism by which GBM cell malignancy is augmented through ARRB1-Δexon13, which mediates glycolysis-related pathways.

Pinocembrin gained novel hepatoprotective properties against cisplatin hepatoxicity through targeting oxidative stress, the crosstalk between TAK1 and inflammatory cascade, and apoptosis. Pinocembrin coadministration with cisplatin might offer a dual benefit on both allied hepatotoxicity and cancer resistance.