ArticleThe Journal of clinical investigation2017
Gα13 ablation reprograms myofibers to oxidative phenotype and enhances whole-body metabolism.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Gα13 Promotes Clonogenic Growth by Increasing Tolerance to Oxidative Metabolic Stress in Prostate Cancer Cells.International journal of molecular sciences · 2025Article
- Effect of castration method on porcine skeletal muscle fiber traits and transcriptome profiles.Veterinary and animal science · 2024Article
- Hepatic Gα13 ablation shifts region-specific colonic inflammatory status by modulating the bile acid synthetic pathway in mice.Scientific reports · 2024Article
- RhoA-mediated GCell discovery · 2024Article
- GPCR-Gα13 Involvement in Mitochondrial Function, Oxidative Stress, and Prostate Cancer.International journal of molecular sciences · 2024Review
- Gα12 and endoplasmic reticulum stress-mediated pyroptosis in a single cycle of dextran sulfate-induced mouse colitis.Scientific reports · 2024Article
- Dysregulated Liver Metabolism and Polycystic Ovarian Syndrome.International journal of molecular sciences · 2023Review
- The spatiotemporal matching pattern of Ezrin/Periaxin involved in myoblast differentiation and fusion and Charcot-Marie-Tooth disease-associated muscle atrophy.Journal of translational medicine · 2023Article
- Targeting the DP2 receptor alleviates muscle atrophy and diet-induced obesity in mice through oxidative myofiber transition.Journal of cachexia, sarcopenia and muscle · 2023Article
- Non-alcoholic fatty liver disease and liver secretome.Archives of pharmacal research · 2022Review
- Article
- GαFrontiers in cell and developmental biology · 2022Review
- Ablation of USP21 in skeletal muscle promotes oxidative fibre phenotype, inhibiting obesity and type 2 diabetes.Journal of cachexia, sarcopenia and muscle · 2021Article
- Article
- Hypergravity Load Modulates Acetaminophen Nephrotoxicity via Endoplasmic Reticulum Stress in Association with Hepatic microRNA-122 Expression.International journal of molecular sciences · 2021Article
- GASC1 promotes hepatocellular carcinoma progression by inhibiting the degradation of ROCK2.Cell death & disease · 2021Article
- GαExperimental & molecular medicine · 2020Review
- miR-208b modulating skeletal muscle development and energy homoeostasis through targeting distinct targets.RNA biology · 2020Article
- G-protein GαScientific reports · 2019Article
- Autotaxin-LPA signaling contributes to obesity-induced insulin resistance in muscle and impairs mitochondrial metabolism.Journal of lipid research · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal muscle is a key organ in energy homeostasis owing to its high requirement for nutrients. Heterotrimeric G proteins converge signals from cell-surface receptors to potentiate or blunt responses against environmental changes. Here, we show that muscle-specific ablation of Gα13 in mice promotes reprogramming of myofibers to the oxidative type, with resultant increases in mitochondrial biogenesis and cellular respiration. Mechanistically, Gα13 and its downstream effector RhoA suppressed nuclear factor of activated T cells 1 (NFATc1), a chief regulator of myofiber conversion, by increasing Rho-associated kinase 2-mediated (Rock2-mediated) phosphorylation at Ser243. Ser243 phosphorylation of NFATc1 was reduced after exercise, but was higher in obese animals. Consequently, Gα13 ablation in muscles enhanced whole-body energy metabolism and increased insulin sensitivity, thus affording protection from diet-induced obesity and hepatic steatosis. Our results define Gα13 as a switch regulator of myofiber reprogramming, implying that modulations of Gα13 and its downstream effectors in skeletal muscle are a potential therapeutic approach to treating metabolic diseases.
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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.