ArticleAutophagy
The heterotrimeric G protein G(i3) regulates hepatic autophagy downstream of the insulin receptor.
Article in Autophagy. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- The κ-opioid receptor-induced autophagy is implicated in stress-driven synaptic alterations.Frontiers in molecular neuroscience · 2022Article
- Lack of GαMolecular metabolism · 2020Article
- The Tnfaip8-PE complex is a novel upstream effector in the anti-autophagic action of insulin.Scientific reports · 2017Article
- Activation of G proteins by GIV-GEF is a pivot point for insulin resistance and sensitivity.Molecular biology of the cell · 2015Article
- Autophagy and apoptosis in liver injury.Cell cycle (Georgetown, Tex.) · 2015Review
- Insulin secretion stimulated by L-arginine and its metabolite L-ornithine depends on Gα(i2).American journal of physiology. Endocrinology and metabolism · 2014Article
- Gαi2 signaling is required for skeletal muscle growth, regeneration, and satellite cell proliferation and differentiation.Molecular and cellular biology · 2014Article
- Article
- A constitutively active Gαi3 protein corrects the abnormal retinal pigment epithelium phenotype of Oa1-/- mice.PloS one · 2013Article
- Gαi2- and Gαi3-specific regulation of voltage-dependent L-type calcium channels in cardiomyocytes.PloS one · 2011Article
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Authors and funding
3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Compelling evidence suggests that the heterotrimeric G protein G(i3) specifically transmits the antiautophagic effects of insulin and amino acids in the liver. This points to a previously unrecognized cross talk between the insulin receptor tyrosine kinase and G(i3). Interestingly, G(i3) is localized not only to plasma membranes but also to membranes of the autophagosomal compartment. Furthermore, as part of insulin's or phenylalanine's actions to inhibit autophagy, G(i3) is redistributed away from autophagosomes. Therefore, endomembrane-associated rather than plasma membrane-localized G(i3) may serve as the target of insulin's endocrine and metabolic actions. We therefore propose that the function and regulation of organelle-associated heterotrimeric G proteins may be different from their roles at the plasma membrane where they act as signal transducers of seven-transmembrane receptors. Here, we discuss recent findings and propose a function for G(i3) in mTOR-dependent signaling pathways. We hypothesize that G(i) family members may have tissue-specific roles in the regulation of autophagy under different physiological and pathological conditions.
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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.