ArticleProceedings of the National Academy of Sciences of the United States of America2007
An obligatory requirement for the heterotrimeric G protein Gi3 in the antiautophagic action of insulin in the liver.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 104 citations in OpenAlex.
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- Cerebrovascular GMolecular imaging and biology · 2023Article
- Impact of interorganelle coordination between the conventional early secretory pathway and autophagy in cellular homeostasis and stress response.Frontiers in cell and developmental biology · 2023Review
- The dual roles of autophagy and the GPCRs-mediating autophagy signaling pathway after cerebral ischemic stroke.Molecular brain · 2022Review
- Gαi protein subunit: A step toward understanding its non-canonical mechanisms.Frontiers in cell and developmental biology · 2022Review
- The Many Faces of G Protein-Coupled Receptor 143, an Atypical Intracellular Receptor.Frontiers in molecular biosciences · 2022Review
- Analyses of Gnai3-iresGFP reporter mice reveal unknown GαScientific reports · 2021Article
- AGS3 and GαMolecules (Basel, Switzerland) · 2020Article
- Lack of GαMolecular metabolism · 2020Article
- Selective protection of murine cerebral GJournal of molecular medicine (Berlin, Germany) · 2020Article
- How to Avoid a No-Deal ER Exit.Cells · 2019Review
- GNAI1 and GNAI3 Reduce Colitis-Associated Tumorigenesis in Mice by Blocking IL6 Signaling and Down-regulating Expression of GNAI2.Gastroenterology · 2019Article
- NFκB mitigates the pathological effects of misfolded α1-antitrypsin by activating autophagy and an integrated program of proteostasis mechanisms.Cell death and differentiation · 2019Article
- Salmonella Typhimurium effector SseI inhibits chemotaxis and increases host cell survival by deamidation of heterotrimeric Gi proteins.PLoS pathogens · 2018Article
- GαOncotarget · 2018Article
- RXFP1 Receptor Activation by Relaxin-2 Induces Vascular Relaxation in MiceFrontiers in physiology · 2018Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Heterotrimeric G proteins of the G(i) class have been implicated in signaling pathways regulating growth and metabolism under physiological and pathophysiological conditions. Knockout mice carrying inactivating mutations in both of the widely expressed Galpha(i) class genes, Galpha(i2) and Galpha(i3), demonstrate shared as well as gene-specific functions. The presence of a single active allele of Galpha(i3) is sufficient for embryonic development, whereas at least one allele of Galpha(i2) is required for extrauterine life. Mice lacking both Galpha(i2) and Galpha(i3) are massively growth-retarded and die in utero. We have used biochemical and cell biological methods together with in situ liver perfusion experiments to study Galpha(i) isoform-specific functions in Galpha(i2)- and Galpha(i3)-deficient mice. The subcellular localization of Galpha(i3) in isolated mouse hepatocytes depends on the cellular metabolic status. Galpha(i3) localizes to autophagosomes upon starvation-induced autophagy and distributes to the plasma membrane upon insulin stimulation. Analysis of autophagic proteolysis in perfused mouse livers showed that mice lacking Galpha(i3) are deficient in the inhibitory action of insulin. These data indicate that Galpha(i3) is crucial for the antiautophagic action of insulin and suggest an as-yet-unrecognized function for Galpha(i3) on autophagosomal membranes.
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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.