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

Subacute SCI is mainly characterized by neuronal apoptosis, axonal demyelination, Wallerian degeneration

They have participated in various cellular processes such as cell proliferation, migration, apoptosis

cellular responses such as proliferation, differentiation, migration, survival, growth, growth arrest and apoptosis ERK-dependent apoptosis as a potential therapeutic strategy for cancer. Cells, 10(10), 2509.

They have participated in various cellular processes such as cell proliferation, migration, apoptosis

In vitro , SACC cell proliferation and apoptosis were evaluated using Cell Counting Kit-8 and colon formation

Cell cycle and apoptosis were determined by flow cytometry.

was involved in the biological process of GPCR signal transduction, hormone metabolism and nerve cell apoptosis

Shh-mediated axon guidance GPCRs in Oncology and Immunology Regulator of G protein signaling 16 restrains apoptosis JNK/p38 MAPK signaling Metallo-protease Peptidase M84 from Bacillusaltitudinis induces ROS-dependent apoptosis

Combinatorial use of AVPR1A and AVPR2 antagonists promoted apoptosis synergistically in CRPC cells.

implicated in myelogenous leukemia where OR2AT4 activation leads to reduced proliferation and enhanced apoptosis In non-small-cell lung cancer OR2J3 activation induced apoptosis and inhibited cell proliferation and

GPCR Activation and Signaling Neuronal survival factor TAFA2 suppresses apoptosis through binding to

Activation of PI3K/Akt pathway by G protein-coupled receptor 37 promotes resistance to cisplatin-induced apoptosis

chidamide synergistically suppresses the proliferation of T-cell lymphoma cells through the enhancement of apoptosis

CircFKBP5 Suppresses Apoptosis and Inflammation and Promotes Osteogenic Differentiation.

Part II: Cell Cycle, DNA Damage Response, and Apoptosis Pathways Spliceosome mutations are associated