GPRC6A (G Protein-Coupled Receptor Class C Group 6 Member A)

We conclude that compound 8h (GRK2/3 inhibitor) and compound 18 (GRK5/6 inhibitor) are highly recommendable tools for the study of GPCR phosphorylation and function in cellular systems. Together, these cell-based GRK inhibitor assays can facilitate medium- to high-throughput screening of future GRK-targeted drug candidates.

The GPCR-TME classifier offers pretreatment predictive value for prognosis and therapeutic responses, potentially enabling novel patient stratification for targeted therapies.

This review comprehensively delineates the expression profiles of GPCRs in GC, their signaling regulatory mechanisms, and dynamic crosstalk with the TME. We critically evaluate the translational value of GPCRs as diagnostic indicators and therapeutic targets, summarize current GPCR-targeted strategies, and propose future research directions to advance precision diagnosis and therapeutic management of GC.

Low-risk patients showed higher sensitivity to AZD6482, BX.795, GDC0941, and pazopanib. GPR176 also modulated the Wnt/β-catenin pathway and M2 macrophage polarization. These findings may provide new insights into the role of orphan class A GPR genes in STAD and identify GPR176 as a new therapeutic target for GC.

The construction of a BC-related GPCR-TME classifier enabled the effective prediction of the OS of BC patients and the identification of SIGMAR1, a key factor regulating ER stress in BC. The knockout of SIGMAR1 can destroy its protective effect on ER stress, enhance apoptosis of BC cells, and facilitate further investigation of novel treatment strategies for cancer therapy.

Further, it discusses emerging therapeutic strategies targeting GPCR signaling pathways to remodel the immunosuppressive TIME in TNBC. These insights into GPCR-mediated immune regulation not only deepen our comprehension of TNBC's pathophysiology but also offer promising avenues for developing novel immunotherapies aimed at enhancing clinical outcomes for TNBC patients.

Dysregulation of GPCR protein expression has been implicated in the pathogenesis of various diseases, including cancer, and GPCR proteins have been shown to modulate these processes in various types of cancer, highlighting their importance as potential therapeutic targets. In this review, we summarize the expression regulation of GPCRs in cancer cells, update the various ways by which the abnormal expression of GPCR protein affects the behavior of tumor cells, and discuss the current research directions and potentially facing problems of strategies on GPCR-targeting therapy.

Further, it discusses emerging therapeutic strategies targeting GPCR signaling pathways to remodel the immunosuppressive TIME in TNBC. These insights into GPCR-mediated immune regulation not only deepen our comprehension of TNBC's pathophysiology but also offer promising avenues for developing novel immunotherapies aimed at enhancing clinical outcomes for TNBC patients.

Furthermore, we explored missense mutations of pediatric ALL in relation to the RNA gene expression findings, providing insights into the genetic underpinnings of this disease. By integrating both RNA-seq and missense mutation data, this article aims to provide an insightful and broader perspective on the potential correlations between specific GPCR and their roles in pediatric ALL.

The remaining nociception could be effectively reversed by PAMAM-Chol-AZ NPs. These findings suggest that PAR2 on oral cancer cells and neurons contribute to oral cancer nociception and NPs loaded with a PAR2 antagonist provide increased antinociception and improved oral function compared to free drug.

Then, GGT1 genotype was also significantly associated with EUS total score and the size of cyst more than 20 mm and more than 30 mm as one of worrisome features of IPMN. Genotypes of carboxypeptidase A1 and gamma-glutamyltransferase 1 may be useful tools for the diagnosis and the predictor of worrisome features of IPMN.

Development of functional imaging targeting aberrant GPCRs should be useful for identification and for specific therapies of this wide spectrum of tumours. The aim of this review is to show that the regulation of endocrine tumours by aberrant GPCR is not restricted to cortisol-secreting adrenal lesions, but also occurs in tumours of several other organs.