ArticleThe Journal of biological chemistry2020
Phosphatidic acid drives mTORC1 lysosomal translocation in the absence of amino acids.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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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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.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Membrane editing with proximity labeling reveals regulators of lipid homeostasis.Nature chemical biology · 2026Article
- Metabolic reprogramming-driven resistance to multi-kinase inhibitors in hepatocellular carcinoma: molecular mechanisms and therapeutic opportunities.Molecular cancer · 2026Review
- The insulin signalling network.Nature metabolism · 2025Review
- The role of phosphatidylcholine metabolism in tumors.Medical oncology (Northwood, London, England) · 2025Review
- Saturated phosphatidic acids induce mTORC1-driven integrated stress response contributing to glucolipotoxicity in hepatocytes.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- mTORC1, the maestro of cell metabolism and growth.Genes & development · 2025Review
- Phosphatidic acid directly activates mTOR and then regulates SREBP to promote ganoderic acid biosynthesis under heat stress in Ganoderma lingzhi.Communications biology · 2024Article
- Effects of phospholipase D1-inhibitory peptide on the growth and metastasis of gastric cancer cells.Molecules and cells · 2024Article
- mTORC1 signaling and diabetic kidney disease.Diabetology international · 2024Review
- mTORC1 Signaling in Brain Endothelial Progenitors Contributes to CCM Pathogenesis.Circulation research · 2024Article
- Activity-based directed evolution of a membrane editor in mammalian cells.Nature chemistry · 2023Article
- Regulation of mTOR by phosphatidic acid.Trends in endocrinology and metabolism: TEM · 2023Review
- Targeting PI3K/AKT/mTOR Pathway in Breast Cancer: From Biology to Clinical Challenges.Biomedicines · 2023Review
- Alcohol, Resistance Exercise, and mTOR Pathway Signaling: An Evidence-Based Narrative Review.Biomolecules · 2022Review
- Targeting mTOR in the Context of Diet and Whole-body Metabolism.Endocrinology · 2022Review
- Click chemistry and optogenetic approaches to visualize and manipulate phosphatidic acid signaling.The Journal of biological chemistry · 2022Article
- Glutaminolysis is involved in the activation of mTORC1 in in vitro-produced porcine embryos.Molecular reproduction and development · 2021Article
- Regulation and metabolic functions of mTORC1 and mTORC2.Physiological reviews · 2021Review
- Review
- The Multifaceted Role of Nutrient Sensing and mTORC1 Signaling in Physiology and Aging.Frontiers in aging · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Mammalian target of rapamycin complex 1 (mTORC1) promotes cell growth and proliferation in response to nutrients and growth factors. Amino acids induce lysosomal translocation of mTORC1 via the Rag GTPases. Growth factors activate Ras homolog enriched in brain (Rheb), which in turn activates mTORC1 at the lysosome. Amino acids and growth factors also induce the phospholipase D (PLD)-phosphatidic acid (PA) pathway, required for mTORC1 signaling through mechanisms that are not fully understood. Here, using human and murine cell lines, along with immunofluorescence, confocal microscopy, endocytosis, PLD activity, and cell viability assays, we show that exogenously supplied PA vesicles deliver mTORC1 to the lysosome in the absence of amino acids, Rag GTPases, growth factors, and Rheb. Of note, pharmacological or genetic inhibition of endogenous PLD prevented mTORC1 lysosomal translocation. We observed that precancerous cells with constitutive Rheb activation through loss of tuberous sclerosis complex subunit 2 (TSC2) exploit the PLD-PA pathway and thereby sustain mTORC1 activation at the lysosome in the absence of amino acids. Our findings indicate that sequential inputs from amino acids and growth factors trigger PA production required for mTORC1 translocation and activation at the lysosome.
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What Socratic holds
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 Socratic graph.