March 2022 ERNEST has established an Emergency Fund for Ukrainian researchers. "General Eligibility Researchers affiliated to any legal entity in Ukraine (for example, schools and universities, research centers, governmental institutions, or private companies) Deadlines Start of the project: now End of the project: 31 October 2022 SHORT-TERM SCIENTIFIC MISSIONS (STSM) We offer short-term scientific mission grants to Ukrainian researchers who have been recently displaced by the war, or those who can travel to institutions participating in ERNEST COST Action. The purpose of the STSM is to carry out a collaborative research project on topics relevant to the network. Our scientific perspective is broad, and we are happy to consider any research proposals from those in need." Read more at the source #DrGPCR #GPCR #IndustryNews

August 2022 Deciphering the signaling mechanisms of β-arrestin1 and β-arrestin2 in regulation of cancer which interact directly and indirectly with a wide number of cellular partners and mediate downstream signaling adaptor proteins that control the recruitment, activation, and scaffolding of numerous cytoplasmic signaling complexes and assist in G-protein receptor signaling, thus bringing them into close proximity. This review delivers a concise overview of the role of β-arrestins with a primary emphasis on the signaling

September 2022 "GPCR signaling and function depend on their associated proteins and subcellular locations they connect a large number of diverse proteins to form signaling networks. We found that some agonist-induced GPCR/14-3-3 signal intensities can rapidly decrease. could also be paralleled with GPCR/β-arrestin-2 signals, indicating diminished levels of GPCR/signal a new approach for GPCR drug development by modulating GPCR/14-3-3 signals temporally."

activity results in the generation of diacylglycerol and inositol trisphosphate, which are downstream signal transducers for the expression of fetal genes, increased protein synthesis, and subsequent cardiomyocyte In this article, we describe the signal transduction elements that regulate PLC gene expression. The discussion is focused on the norepinephrine- α1-adrenoceptor signaling pathway and downstream signaling the expression of PLC isozymes with the suggestion that PLC activities may be part of a coordinated signaling

bound to these interaction partners available today do not reveal a clear conformational basis for signaling orientation of individual residues and/or their interactions not easily detectable in the receptor-transducer binding to different types of partners rather than the structures of the final complexes might underlie transducer

When it comes to signal transduction, cellular context matters. to scaffold various kinases and modulate downstream signaling pathways. can be activated by ligands and initiate signaling cascades. , sustained signaling responses from intracellular compartments can be regulated by the kinetics of signaling Compartmentalized GPCR Signaling from Intracellular Membranes.

Furthermore, in sPD models, the shortening of PC is accompanied by increased Sonic Hedgehog (SHH) signal transduction. Inhibiting overactive SHH signaling may be a potential neuroprotective therapy for sPD."

protein-coupled receptors (GPCRs) are membrane-bound proteins that sense external stimuli and relay signals For example, dimerization has been shown to affect signaling pathways in class A dopamine receptors like decreased high-affinity binding to its natural ligand, GLP-1, while selectively affecting receptor signaling transduction. Perreault, M.L., et al., Heteromeric dopamine receptor signaling complexes: emerging neurobiology and

correlate with three cholesterol molecules that play essential roles in conformation stabilization and signaling transduction. Thus, our data deepen the understanding of cholesterol modulation in GPCR (G protein-coupled receptor) signaling

Opioid receptors belong to class A of G protein-coupled receptors or GPCRs and signaled mainly through Therefore, the study of the different signal transductions triggered by the opioid-receptor interaction downstream through different signaling pathways triggered by different molecules2. There are several reports that have addressed the differences in the mechanisms of transduction triggered Therefore to understand better the functions of arrestins in MOR signaling, Shiraki et al., explored

greater understanding of how effector molecules interact with a receptor to initiate downstream effector signaling This review aims to explore the signaling pathways, dynamic structures, and physiological relevance in the cardiovascular system of the three most important GPCR signaling effectors: heterotrimeric G proteins is increasing appreciation for the elegance of the regulatory mechanisms that mediate intracellular signaling

Calcium (Ca2+) signaling is known to direct processes that govern chondrocyte gene expression, protein Control of chondrocyte/chondroprogenitor Ca2+ signaling has been attempted through mechanical and/or pharmacological activation of endogenous Ca2+ signaling transducers; however, such approaches can lack Synthetic signaling platforms permitting precise and selective Ca2+ signal transduction can improve dissection of the roles that [Ca2+]i signaling plays in chondrocyte behavior.

G protein-coupled receptors (GPCRs) activation assumes that stimulation of heterotrimeric G protein signaling In this model, GPCR signaling is turned-off by receptor phosphorylation via GPCR kinases (GRKs) and subsequent the last decade, this model has been extended by discovering that some internalized GPCRs continue to signal Accumulative evidence shows that the location of signaling has an impact on the physiological effects of GPCR signaling.

Regulator G protein Signaling (RGS) proteins are critical components of the intracellular signaling pathways and amplitude of GPCR signaling. Another signaling pathway related to RGS4 involves the regulation of the immune response. Senese, N.B., et al., Regulator of G-Protein Signaling (RGS) Protein Modulation of Opioid Receptor Signaling Hepler, Cellular regulation of RGS proteins: modulators and integrators of G protein signaling.

protein-coupled receptors (GPCRs) are integral membrane proteins crucial for sensing extracellular signals These receptors initiate intracellular signaling cascades upon activation, ultimately regulating a myriad due to pathway crosstalk and signal amplification [3]. Gilman, A.G., G proteins: transducers of receptor-generated signals.  Salahpour, A., et al., BRET biosensors to study GPCR biology, pharmacology, and signal transduction. 

How this HR is involved in hormone binding and signal transduction is still an open question. The models are expected to allow for testable hypotheses about signal transduction and drug development

regulation of mTORC1 by upstream stimuli, with a specific focus on G-protein coupled receptor (GPCR) signaling

October 2022 High hedgehog signaling is transduced by a multikinase-dependent switch controlling the distribution of the GPCR smoothened "The oncogenic G-protein-coupled receptor (GPCR) Smoothened (SMO) is a key transducer

We will discuss recent evidence as well as what we consider as emerging areas to explore; from the signalling relevance of these interactions, since this additional level of molecular cross-talk between receptors and signaling

Rho1 signaling is activated by G-protein-coupled receptor (GPCR) signaling at the cell surface. embryonic salivary gland (SG) invagination, the GPCR ligand Folded gastrulation (Fog) activates Rho1 signaling The SG receptor that transduces the Fog signal into Rho1-dependent myosin activation has not been identified Here, we reveal that the Smog GPCR transduces Fog signal to regulate Rho kinase accumulation and myosin

Rho1 signaling is activated by G-protein-coupled receptor (GPCR) signaling at the cell surface. embryonic salivary gland (SG) invagination, the GPCR ligand Folded gastrulation (Fog) activates Rho1 signaling The SG receptor that transduces the Fog signal into Rho1-dependent myosin activation has not been identified Here, we reveal that the Smog GPCR transduces Fog signal to regulate Rho kinase accumulation and myosin

Through bioinformatic analysis of lysosomal proteomes, we identified lysosomal cholesterol signaling pathway for cholesterol sensing and couples cholesterol concentrations to mTORC1-dependent anabolic signaling

One fascinating aspect of the cellular signaling network is the crosstalk between G protein-coupled receptors while promoting constitutive Gβγ signaling. localization and signaling efficiency. intervention in diseases characterized by dysregulated signaling pathways. Science signaling, 17(839), eade8041. https://doi.org/10.1126/scisignal.ade8041

vast family of membrane-bound proteins crucial for transmitting external stimuli into intracellular signals Gi/o, Gq/11, and G12/13, at the initial GPCR-G protein association step, ensuring precise downstream signalling Instead, G12 overexpression inhibited V2R downstream signalling, including β-arrestin recruitment and This unproductive coupling revealed that non-cognate G protein interactions could modulate GPCR signalling Gupte, T.M., et al., Priming GPCR signaling through the synergistic effect of two G proteins. 

Integration and Spatial Organization of Signaling by G Protein-Coupled Receptor Homo- and Heterodimer Information flow from a source to a receiver becomes informative when the recipient can process the signal Information exchange and interpretation is essential in biology and understanding how cells integrate signals communication occurs mostly through neurotransmitters and hormones, and receptors are responsible for signal recognition at the membrane level and information transduction inside the cell.

October 2022 Genome-scale CRISPR screening reveals that C3aR signaling is critical for rapid capture

applications of Nbs to facilitate the development of more selective drugs capable of modulating specific signaling

September 2022 Biased GPCR signaling by the native parathyroid hormone-related protein 1 to 141 relative splice variants of 139, 141, and 173 amino acids, our current understanding on how endogenous PTHrP transduces signals through its cognate G-protein coupled receptor (GPCR), the PTH type 1 receptor (PTHR), is largely Furthermore, we show that the molecular basis for biased signaling differences between PTHrP1-36 and Taken together, our results contribute to a better understanding of the biased signaling process of a