ArticleNature communications2020
mTORC2-AKT signaling to ATP-citrate lyase drives brown adipogenesis and de novo lipogenesis.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 92 papers.
What it found
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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.
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Who cites it
92 citing papers in PubMed, 147 citations in OpenAlex.
- Article
- New insights into the ACLY-mediated metabolic and epigenetic interplay in macrophages.Journal of enzyme inhibition and medicinal chemistry · 2026Review
- How mitochondrial heterogeneity fuels a dynamic organelle ecosystem.Communications biology · 2026Review
- Non-enzymatic hepatic ABHD6 interacts with Akt-FoxO1 axis to regulate metabolic health.Nature communications · 2026Article
- PFAS Exposure and Metabolic Disorders: Mechanistic Insights into Lipid and Glucose Homeostasis.Biomolecules · 2026Review
- ACLY integrates metabolism and chromatin accessibility to enable B Cell activation and humoral immunity.bioRxiv : the preprint server for biology · 2026Article
- ChREBP-mediated regulation of lipid metabolism in liver and brown adipose tissue of long-lived mice.GeroScience · 2026Article
- Functional and metabolomic analyses of brown adipose tissue during cold-deacclimation reveal rapid N-acetylated amino acid adaptations.iScience · 2026Article
- Type 2 Diabetes Mellitus as a Multisystem Disease: From Insulin Resistance to Organ Crosstalk-A Narrative Review.Biomedicines · 2026Review
- Signalling pathways in hepatocellular carcinoma (HCC) metastasis and invasion: Molecular mechanisms and therapeutic implications.Biochemistry and biophysics reports · 2026Review
- Non-enzymatic ABHD6 interacts with Akt-FoxO1 axis to regulate selective hepatic insulin resistance.bioRxiv : the preprint server for biology · 2026Article
- Liprin-α1 enhances PHLDB3 oncogenic function in colorectal cancer via activation of mTORC2-AKT1 pathway.Cell reports · 2026Article
- The UFL1-AKT positive feedback loop promotes breast cancer progression by enhancing lipid synthesis.Nature communications · 2026Article
- Maternal monosodium glutamate exposure disrupts leptin and insulin signaling in the hypothalamus, activating NF-κB and mTOR inflammatory pathways, contributing to metabolic dysfunction in male offspring.International journal of obesity (2005) · 2026Article
- PDGFRαAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Heart-guarding or heart-harming? The dual role of epicardial adipose tissue in cardiovascular health and disease.International journal of obesity (2005) · 2025Review
- Discovery and mechanism of a highly selective, antifungal acetyl-CoA synthetase inhibitor.Nature communications · 2025Article
- Phosphorylation of USP33 by CDK1 stabilizes the mTORC2 component SIN1.Cell death & disease · 2025Article
- PI3Kβ moonlights as a protein kinase: driving fatty acid metabolism and histone acetylation in cancer.Cancer biology & medicine · 2025Article
- Mechanotransduction for therapeutic approaches: Cellular aging and rejuvenation.APL bioengineering · 2025Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
mTORC2 phosphorylates AKT in a hydrophobic motif site that is a biomarker of insulin sensitivity. In brown adipocytes, mTORC2 regulates glucose and lipid metabolism, however the mechanism has been unclear because downstream AKT signaling appears unaffected by mTORC2 loss. Here, by applying immunoblotting, targeted phosphoproteomics and metabolite profiling, we identify ATP-citrate lyase (ACLY) as a distinctly mTORC2-sensitive AKT substrate in brown preadipocytes. mTORC2 appears dispensable for most other AKT actions examined, indicating a previously unappreciated selectivity in mTORC2-AKT signaling. Rescue experiments suggest brown preadipocytes require the mTORC2/AKT/ACLY pathway to induce PPAR-gamma and establish the epigenetic landscape during differentiation. Evidence in mature brown adipocytes also suggests mTORC2 acts through ACLY to increase carbohydrate response element binding protein (ChREBP) activity, histone acetylation, and gluco-lipogenic gene expression. Substrate utilization studies additionally implicate mTORC2 in promoting acetyl-CoA synthesis from acetate through acetyl-CoA synthetase 2 (ACSS2). These data suggest that a principal mTORC2 action is controlling nuclear-cytoplasmic acetyl-CoA synthesis.
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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.