ArticlePloS one2013
Normal autophagic activity in macrophages from mice lacking Gαi3, AGS3, or RGS19.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Myeloid GPSM1 regulates atherosclerosis progression by governing monocyte and macrophage activation and chemotaxis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Identification of Potential Diagnoses Based on Immune Infiltration and Autophagy Characteristics in Major Depressive Disorder.Frontiers in genetics · 2022Article
- Intersection of two key signal integrators in the cell: activator of G-protein signaling 3 and dishevelled-2.Journal of cell science · 2020Article
- GαJournal of immunology (Baltimore, Md. : 1950) · 2019Article
- Role of G-proteins and phosphorylation in the distribution of AGS3 to cell puncta.Journal of cell science · 2018Article
- Genetic Analysis of Rare Human Variants of Regulators of G Protein Signaling Proteins and Their Role in Human Physiology and Disease.Pharmacological reviews · 2018Review
- 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
- Activators of G protein signaling in the kidney.The Journal of pharmacology and experimental therapeutics · 2015Review
- Implications of non-canonical G-protein signaling for the immune system.Cellular signalling · 2014Review
- Review
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Authors and funding
9 authors at 4 institutions in 1 country.
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Abstract
In macrophages autophagy assists antigen presentation, affects cytokine release, and promotes intracellular pathogen elimination. In some cells autophagy is modulated by a signaling pathway that employs Gαi3, Activator of G-protein Signaling-3 (AGS3/GPSM1), and Regulator of G-protein Signaling 19 (RGS19). As macrophages express each of these proteins, we tested their importance in regulating macrophage autophagy. We assessed LC3 processing and the formation of LC3 puncta in bone marrow derived macrophages prepared from wild type, Gnai3(-/-), Gpsm1(-/-), or Rgs19(-/-) mice following amino acid starvation or Nigericin treatment. In addition, we evaluated rapamycin-induced autophagic proteolysis rates by long-lived protein degradation assays and anti-autophagic action after rapamycin induction in wild type, Gnai3(-/-), and Gpsm1(-/-) macrophages. In similar assays we compared macrophages treated or not with pertussis toxin, an inhibitor of GPCR (G-protein couple receptor) triggered Gαi nucleotide exchange. Despite previous findings, the level of basal autophagy, autophagic induction, autophagic flux, autophagic degradation and the anti-autophagic action in macrophages that lacked Gαi3, AGS3, or RGS19; or had been treated with pertussis toxin, were similar to controls. These results indicate that while Gαi signaling may impact autophagy in some cell types it does not in macrophages.
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