ArticleMolecular and cellular biology2010
Distribution of activator of G-protein signaling 3 within the aggresomal pathway: role of specific residues in the tetratricopeptide repeat domain and differential regulation by the AGS3 binding partners Gi(alpha) and mammalian inscuteable.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 28 citations in OpenAlex.
- β-arrestin recruitment facilitates a direct association with G proteins.Nature communications · 2026Article
- A homozygous frameshift variant in the CILK1 gene causes cranioectodermal dysplasia.European journal of human genetics : EJHG · 2025Article
- CilioGenics: an integrated method and database for predicting novel ciliary genes.Nucleic acids research · 2024Article
- Properties of biomolecular condensates defined by Activator of G-protein Signaling 3.Journal of cell science · 2024Article
- Activators of G-Protein Signaling 3 (AGS3) Puncta: Potential Novel Biomolecular Condensates in Signal Transduction.Journal of cell science & therapy · 2024Article
- Intersection of two key signal integrators in the cell: activator of G-protein signaling 3 and dishevelled-2.Journal of cell science · 2020Article
- Activator of G protein signaling 3 modulates prostate tumor development and progression.Carcinogenesis · 2019Article
- Role of G-proteins and phosphorylation in the distribution of AGS3 to cell puncta.Journal of cell science · 2018Article
- Activator of G-Protein Signaling 3-Induced Lysosomal Biogenesis Limits Macrophage Intracellular Bacterial Infection.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Direct Coupling of a Seven-Transmembrane-Span Receptor to a Gαi G-Protein Regulatory Motif Complex.Molecular pharmacology · 2015Article
- Gαi3-Dependent Inhibition of JNK Activity on Intracellular Membranes.Frontiers in bioengineering and biotechnology · 2015Article
- Canonical and noncanonical g-protein signaling helps coordinate actin dynamics to promote macrophage phagocytosis of zymosan.Molecular and cellular biology · 2014Article
- Defective chemokine signal integration in leukocytes lacking activator of G protein signaling 3 (AGS3).The Journal of biological chemistry · 2014Article
- Activators of G protein signaling exhibit broad functionality and define a distinct core signaling triad.Molecular pharmacology · 2014Review
- Translocation of activator of G-protein signaling 3 to the Golgi apparatus in response to receptor activation and its effect on the trans-Golgi network.The Journal of biological chemistry · 2013Article
- Differential effects of AGS3 expression on D(2L) dopamine receptor-mediated adenylyl cyclase signaling.Cellular and molecular neurobiology · 2013Article
- Regulation of the G-protein regulatory-Gαi signaling complex by nonreceptor guanine nucleotide exchange factors.The Journal of biological chemistry · 2013Article
- Article
- The G-protein regulator LGN modulates the activity of the NO receptor soluble guanylate cyclase.The Biochemical journal · 2012Article
- Misfolded Gβ is recruited to cytoplasmic dynein by Nudel for efficient clearance.Cell research · 2012Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
AGS3, a receptor-independent activator of G-protein signaling, is involved in unexpected functional diversity for G-protein signaling systems. AGS3 has seven tetratricopeptide (TPR) motifs upstream of four G-protein regulatory (GPR) motifs that serve as docking sites for Gialpha-GDP. The positioning of AGS3 within the cell and the intramolecular dynamics between different domains of the proteins are likely key determinants of their ability to influence G-protein signaling. We report that AGS3 enters into the aggresome pathway and that distribution of the protein is regulated by the AGS3 binding partners Gialpha and mammalian Inscuteable (mInsc). Gialpha rescues AGS3 from the aggresome, whereas mInsc augments the aggresome-like distribution of AGS3. The distribution of AGS3 to the aggresome is dependent upon the TPR domain, and it is accelerated by disruption of the TPR organizational structure or introduction of a nonsynonymous single-nucleotide polymorphism. These data present AGS3, G-proteins, and mInsc as candidate proteins involved in regulating cellular stress associated with protein-processing pathologies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.