August 2022 Deciphering the signaling mechanisms of β-arrestin1 and β-arrestin2 in regulation of cancer cell cycle and metastasis "β-Arrestins are ubiquitously expressed intracellular proteins with many functions They have participated in various cellular processes such as cell proliferation, migration, apoptosis

Inhibition of autophagy by 3-methyladenine or interference of ATG5 or ATG7 attenuated HBx-induced cell cycle acceleration and the subsequent proliferative response via the induction of G1/S arrest. protein kinase; ATG5: autophagy related 5; ATG7: autophagy related 7; Baf A1: bafilomycin A1; CDK2: cyclin dependent kinase 2; CDKN1B/p27Kip1: cyclin dependent kinase inhibitor 1B; CQ: chloroquine; E2F1: E2F

Data by Arne Hansen et a l has introduced a sensitive method for detecting GPCR mRNAs in human immune cells The study reports that human white blood cells express an average of 160 GPCR mRNAs, ranging from 123 , suggesting a potential role in regulating red blood cell production and offering a novel avenue for Additionally, the study identified unique expression patterns of GPCRs in different immune cell types , including B cells, CD4+ T cells, CD8+ T cells, natural killer (NK) cells, and dendritic cells.

Among the five somatostatin receptors, SST2 and SST3 are associated with apoptosis and cell cycle arrest and SST3 reemerged in metastases suggesting conserved receptors genetic potential during tumor life cycle Michel Afargan Source Contribute to the GPCR News Coming soon Become a Contributor Classified GPCR News Call

Registration Logo Contest Committee Sponsors GPCR Retreat Program < Back to schedule Interaction with the cell adhesion molecule NEGR1 affects mGluR5 cell signalling Date & Time Friday, November 3rd / 1:30 PM Abstract Ribeiro has supervised eleven M.Sc. and six Ph.D. students, as well as five post-doctorate fellows. Nowadays, her research group comprises four undergraduates, two M.Sc., and six Ph.D. students, as well These drugs were shown to be very effective to rescue the cell death observed in a mouse model of Huntington

Design: We analyzed the effects of one GPCR coexpressed with CCR5, EBI2, on HIV-1 replicative cycle. Methods: We identified GPCRs expressed in primary CD4+CCR5+ T cells by multi-RT-qPCR. Cell lines expressing EBI2 were established by transduction with HIV vectors. The amount of HIV reverse transcripts was similar in cells expressing or not EBI2. Conclusions: EBI2 expression in CD4+CCR5+ cells boosts HIV-1 R5 productive infection.