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Activator of G-protein Signaling 3 is an important regulator of esophageal squamous cell carcinoma proliferation
Results confirmed that Ric-8A (show RIC8A ELISA Kits) can directly bind to AGS3S but failed to facilitate Galpha (show SUCLG1 ELISA Kits)(i)-induced suppression of adenylyl cyclase, suggesting that it may not serve as a guanine exchange factor for AGS3/Galpha (show SUCLG1 ELISA Kits)(i/o)-GDP complex in a cellular environment.
High GPSM1 gene methylation is associated with gastric tumor aggressiveness.
Data identified three new loci for type 2 diabetes with genome-wide significance: MIR129-LEP (show LEP ELISA Kits), GPSM1 and SLC16A13 (show SLC16A13 ELISA Kits).
Our data indicate that decreased expression of AGS3 is correlated with reduced levels of p-CREB (show CREB1 ELISA Kits) in the apoptotic model. The negative role of AGS3 in cell apoptosis was further confirmed by knocking down AGS3.
these results indicate that GRK6 (show GRK6 ELISA Kits) complexes with AGS3-Galphai2 (show GNAI2 ELISA Kits) to regulate CXCR2 (show CXCR2 ELISA Kits)-mediated leukocyte functions at different levels, including downstream effector activation, receptor trafficking, and expression at the cell membrane.
These results provide mechanistic insights into how reversible modulation of Galpha (show SUCLG1 ELISA Kits)(i3) activity by AGS3 and GIV (show CCDC88A ELISA Kits) maintains the delicate equilibrium between promotion and inhibition of autophagy.
AGS3 receptor coupling to both Galphabetagamma and GPR (show ALDH18A1 ELISA Kits)-Galpha (show SUCLG1 ELISA Kits)(i) offer additional flexibility for systems to respond and adapt to challenges and orchestrate complex behaviors
unlike wild-type AGS3, over-expression of an AGS3 mutant lacking this modification fails to enhance macroautophagic activity. These observations imply that AGS3 phosphorylation may participate in the modulation of macroautophagy
These data present AGS3, G-proteins, and mInsc as candidate proteins involved in regulating cellular stress associated with protein-processing pathologies.
We conclude that LPS (show TLR4 ELISA Kits) priming increases AGS3 levels, which enhances lysosomal function and increases the capacity of macrophages to eliminate intracellular pathogens.
level of basal autophagy, autophagic induction, autophagic flux, autophagic degradation and the anti-autophagic action in macrophages that lacked Galphai3 (show GNAI3 ELISA Kits), AGS3, or RGS19 (show RGS19 ELISA Kits); or had been treated with pertussis toxin, were similar to controls
AGS3 has a role in the regulation of G-protein signaling in the immune system
The present study demonstrates an important role for GPSM1 in controlling the dynamics of cyst progression in an orthologous mouse model of autosomal dominant polycystic kidney disease.
These data suggest that Gpsm1 acts through a novel receptor-independent mechanism to facilitate renal tubular epithelial cell proliferation and renal tubular regeneration.
AGS3 null mice exhibited a lean phenotype, reduced fat mass, and increased nocturnal energy expenditure.
The GPR (show ALDH18A1 ELISA Kits) motif in this protein and other proteins is actually associated with activity as a GDI - guanine nucleotide dissociation inhibitor and not GTPase (show RACGAP1 ELISA Kits) activator as initially suggested.
G-protein signaling modulators (GPSMs) play diverse functional roles through their interaction with G-protein subunits. This gene encodes a receptor-independent activator of G protein signaling, which is one of several factors that influence the basal activity of G-protein signaling systems. The protein contains seven tetratricopeptide repeats in its N-terminal half and four G-protein regulatory (GPR) motifs in its C-terminal half. Multiple alternatively spliced transcript variants encoding different isoforms have been found for this gene.
G-protein signalling modulator 1 (AGS3-like, C. elegans)
, G-protein-signaling modulator 1
, activator of G-protein signaling 3
, G-protein signaling modulator 1 (AGS3-like, C. elegans)