ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011
Loss of activator of G-protein signaling 3 impairs renal tubular regeneration following acute kidney injury in rodents.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 48 citations in OpenAlex.
- Molecular insights into AGS3's role in spindle orientation: a biochemical perspective.Journal of molecular cell biology · 2025Article
- Genetic background in the rat affects endocrine and metabolic outcomes of bisphenol F exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- Liquid Biopsy at the Frontier of Kidney Diseases: Application of Exosomes in Diagnostics and Therapeutics.Genes · 2023Review
- Article
- Knockdown of GPSM1 Inhibits the Proliferation and Promotes the Apoptosis of B-Cell Acute Lymphoblastic Leukemia Cells by Suppressing the ADCY6-RAPGEF3-JNK Signaling Pathway.Pathology oncology research : POR · 2021Article
- Intersection of two key signal integrators in the cell: activator of G-protein signaling 3 and dishevelled-2.Journal of cell science · 2020Article
- Activation of the cannabinoid receptor 2 increases renal perfusion.Physiological genomics · 2019Article
- Role of G-proteins and phosphorylation in the distribution of AGS3 to cell puncta.Journal of cell science · 2018Article
- Urinary exosomal expression of activator of G protein signaling 3 in polycystic kidney disease.BMC research notes · 2018Article
- Polycystin 1 loss of function is directly linked to an imbalance in G-protein signaling in the kidney.Development (Cambridge, England) · 2018Article
- Selective Cannabinoid 2 Receptor Stimulation Reduces Tubular Epithelial Cell Damage after Renal Ischemia-Reperfusion Injury.The Journal of pharmacology and experimental therapeutics · 2018Article
- Targeting GPCR-Gβγ-GRK2 signaling as a novel strategy for treating cardiorenal pathologies.Biochimica et biophysica acta. Molecular basis of disease · 2017Review
- TRIP13-deficient tubular epithelial cells are susceptible to apoptosis following acute kidney injury.Scientific reports · 2017Article
- Regulation of Chemokine Signal Integration by Activator of G-Protein Signaling 4 (AGS4).The Journal of pharmacology and experimental therapeutics · 2017Article
- Hexavalent chromium induces expression of mesenchymal and stem cell markers in renal epithelial cells.Molecular carcinogenesis · 2016Article
- Activator of G-Protein Signaling 3-Induced Lysosomal Biogenesis Limits Macrophage Intracellular Bacterial Infection.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Activator of G-protein Signaling 3 Controls Renal Epithelial Cell Survival and ERK5 Activation.Journal of molecular signaling · 2015Article
- B Lymphocyte-Specific Loss of Ric-8A Results in a Gα Protein Deficit and Severe Humoral Immunodeficiency.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Direct Coupling of a Seven-Transmembrane-Span Receptor to a Gαi G-Protein Regulatory Motif Complex.Molecular pharmacology · 2015Article
- Activators of G protein signaling in the kidney.The Journal of pharmacology and experimental therapeutics · 2015Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The intracellular mechanisms underlying renal tubular epithelial cell proliferation and tubular repair following ischemia-reperfusion injury (IRI) remain poorly understood. In this report, we demonstrate that activator of G-protein signaling 3 (AGS3), an unconventional receptor-independent regulator of heterotrimeric G-protein function, influences renal tubular regeneration following IRI. In rat kidneys exposed to IRI, there was a temporal induction in renal AGS3 protein expression that peaked 72 h after reperfusion and corresponded to the repair and recovery phase following ischemic injury. Renal AGS3 expression was localized predominantly to the recovering outer medullary proximal tubular cells and was highly coexpressed with Ki-67, a marker of cell proliferation. Kidneys from mice deficient in the expression of AGS3 exhibited impaired renal tubular recovery 7 d following IRI compared to wild-type AGS3-expressing mice. Mechanistically, genetic knockdown of endogenous AGS3 mRNA and protein in renal tubular epithelial cells reduced cell proliferation in vitro. Similar reductions in renal tubular epithelial cell proliferation were observed following incubation with gallein, a selective inhibitor of Gβγ subunit activity, and lentiviral overexpression of the carboxyl-terminus of G-protein-coupled receptor kinase 2 (GRK2ct), a scavenger of Gβγ subunits. In summary, these data suggest that AGS3 acts through a novel receptor-independent mechanism to facilitate renal tubular epithelial cell proliferation and renal tubular regeneration.
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