Deficiency of β-arrestin2 alleviates apoptosis through GRP78-ATF6-CHOP signaling pathway in primary Sjögren's In vivo, we found that inhibition of GRP78-ATF6-CHOP apoptosis signaling improved ESS symptoms, and the apoptosis, and the effect depended on the interaction between GRP78 and β-arrestin2. in the pathogenesis of pSS and that β-arrestin2 encourages inflammation-induced epithelial apoptosis through GRP78-ATF6-CHOP apoptosis signaling.

September 2022 "Research on cancer therapies focuses on processes such as angiogenesis, cell signaling, stemness, metastasis, and drug resistance and inflammation, all of which are influenced by the cellular and molecular microenvironment of the tumor. Different strategies, such as antibodies, small chemicals, hormones, cytokines, and, recently, gene editing techniques, have been tested to reduce the malignancy and generate a harmful microenvironment for the tumor. Few therapeutic agents have shown benefits when administered alone, but a few more have demonstrated clear improvement when administered in combination with other therapeutic molecules. In 2008 (and for the first time in the clinic), the therapeutic benefits of the β-adrenergic receptor antagonist, propranolol, were described in benign tumors, such as infantile hemangioma. Propranolol, initially prescribed for high blood pressure, irregular heart rate, essential tremor, and anxiety, has shown, in the last decade, increasing evidence of its antitumoral properties in more than a dozen different types of cancer. Moreover, the use of propranolol in combination therapies with other drugs has shown synergistic antitumor effects. This review highlights the clinical trials in which propranolol is taking part as adjuvant therapy at single administration or in combinatorial human trials, arising as a good pick and roll partner in anticancer strategies." Read more at the source #DrGPCR #GPCR #IndustryNews

Methods Proliferation, migration and apoptosis assays were performed in ovarian cancer cells after

Oncology and Immunology Metallo-protease Peptidase M84 from Bacillusaltitudinis induces ROS-dependent apoptosis This metallo-protease had no discernible impact on normal cell survival, but it specifically induced apoptosis This evoked apoptotic death of the ovarian cancer cells through the intrinsic route. Collectively, our findings suggested that Peptidase M84 triggered PAR-1-mediated oxidative stress to act as an apoptosis

< GPCR News < GPCRs in Oncology and Immunology CircFKBP5 Suppresses Apoptosis and Inflammation and Promotes Materials and methods: The viability and apoptosis of human DPSCs (hDPSCs) were determined using Cell expression was decreased in hDPSCs and, functionally, reexpression of circFKBP5 attenuated LPS-induced apoptosis Conclusions: CircFKBP5 could protect against LPS-induced apoptosis, inflammation, and osteogenic differentiation

Activation of PI3K/Akt pathway by G protein-coupled receptor 37 promotes resistance to cisplatin-induced apoptosis Furthermore, we examined the effects of GPR37 on tumor cell apoptosis and invasion. that GPR37 positively regulates NSCLC cell invasion, migration, and proliferation, suppresses cell apoptosis observed that GPR37 knockdown suppresses NSCLC cell invasion, migration, and proliferation, promotes cell apoptosis