ArticleAmerican journal of physiology. Cell physiology2010
Phosphatidic acid mediates activation of mTORC1 through the ERK signaling pathway.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 82 citations in OpenAlex.
- The effects of phosphatidic acid supplementation on strength, body composition, muscular endurance, power, agility, and vertical jump in resistance trained men.Journal of the International Society of Sports Nutrition · 2016Trial
- Article
- Phosphatidic Acid-TRIM59-Olig2 Signaling Couples Metabolic Dysfunction to Myelination Failure in PWMI.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Lipidomic profiling of endometrial cancer using desorption electrospray ionization mass spectrometry imaging.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- DGKs in lipid signaling and disease intervention: structural basis, pathological mechanisms, and emerging therapeutic strategies.Cellular & molecular biology letters · 2025Review
- The MDA-MB-231 Breast Cancer Cell Secretomes Modify Metabolomes ofInternational journal of molecular sciences · 2025Article
- Ultralow Background Membrane Editors for Spatiotemporal Control of Phosphatidic Acid Metabolism and Signaling.ACS central science · 2024Article
- Oleic acid stimulation of amino acid uptake in primary human trophoblast cells is mediated by phosphatidic acid and mTOR signaling.FASEB bioAdvances · 2024Article
- Ultralow background membrane editors for spatiotemporal control of lipid metabolism and signaling.bioRxiv : the preprint server for biology · 2023Article
- Review
- Optical Control of Phosphatidic Acid Signaling.ACS central science · 2021Article
- Phosphatidic Acid Stimulates Myoblast Proliferation through Interaction with LPA1 and LPA2 Receptors.International journal of molecular sciences · 2021Article
- The Roles of Lpar1 in Central Nervous System Disorders and Diseases.Frontiers in neuroscience · 2021Review
- MYC-binding lncRNA EPIC1 promotes AKT-mTORC1 signaling and rapamycin resistance in breast and ovarian cancer.Molecular carcinogenesis · 2020Article
- Beyond Lipid Signaling: Pleiotropic Effects of Diacylglycerol Kinases in Cellular Signaling.International journal of molecular sciences · 2020Review
- Ovary removal modifies liver message RNA profiles in single Comb White Leghorn chickens.Poultry science · 2020Article
- Phospholipase D2 in prostate cancer: protein expression changes with Gleason score.British journal of cancer · 2019Article
- Review
- Lipin deactivation after acetaminophen overdose causes phosphatidic acid accumulation in liver and plasma in mice and humans and enhances liver regeneration.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2018Article
- Targeting the mesenchymal subtype in glioblastoma and other cancers via inhibition of diacylglycerol kinase alpha.Neuro-oncology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The mammalian target of rapamycin (mTOR) assembles into two distinct multiprotein complexes known as mTORC1 and mTORC2. Of the two complexes, mTORC1 acts to integrate a variety of positive and negative signals to downstream targets that regulate cell growth. The lipid second messenger, phosphatidic acid (PA), represents one positive input to mTORC1, and it is thought to act by binding directly to mTOR, thereby enhancing the protein kinase activity of mTORC1. Support for this model includes findings that PA binds directly to mTOR and addition of PA to the medium of cells in culture results in activation of mTORC1. In contrast, the results of the present study do not support a model in which PA activates mTORC1 through direct interaction with the protein kinase but, instead, show that the lipid promotes mTORC1 signaling through activation of the ERK pathway. Moreover, rather than acting directly on mTORC1, the results suggest that exogenous PA must be metabolized to lysophosphatidic acid (LPA), which subsequently activates the LPA receptor endothelial differentiation gene (EDG-2). Finally, in contrast to previous studies, the results of the present study demonstrate that leucine does not act through phospholipase D and PA to activate mTORC1 and, instead, show that the two mediators act through parallel upstream signaling pathways to activate mTORC1. Overall, the results demonstrate that leucine and PA signal through parallel pathways to activate mTORC1 and that PA mediates its effect through the ERK pathway, rather than through direct binding to mTOR.
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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.