ArticleeLife2013
Massive endocytosis triggered by surface membrane palmitoylation under mitochondrial control in BHK fibroblasts.
Article in eLife, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 78 citations in OpenAlex.
- Functional Specialization of Clathrin-Independent Endocytic Routes: Mechanisms and Cellular Roles.Traffic (Copenhagen, Denmark) · 2026Review
- Palmitoylation calibrates mitochondrial transport of insulin across the endothelium in insulin resistance.bioRxiv : the preprint server for biology · 2026Article
- Molecular regulation and physiological role of GOLPH3-mediated Golgi retention.Nature communications · 2026Article
- Palmitic acid and palmitoylation in cancer: Understanding, insights, and challenges.Innovation (Cambridge (Mass.)) · 2025Review
- Protein lipidation in the tumor microenvironment: enzymology, signaling pathways, and therapeutics.Molecular cancer · 2025Review
- Protein palmitoylation: an emerging regulator of inflammatory signaling and diseases.Frontiers in immunology · 2025Review
- Membrane lipid nanodomains modulate HCN pacemaker channels in nociceptor DRG neurons.Nature communications · 2024Article
- The endolysosomal system in conventional and unconventional protein secretion.The Journal of cell biology · 2024Review
- Constitutive Plasma Membrane Turnover in T-REx293 cells via Ordered Membrane Domain Endocytosis under Mitochondrial Control.bioRxiv : the preprint server for biology · 2024Article
- Ferroptosis in liver cancer: a key role of post-translational modifications.Frontiers in immunology · 2024Review
- Massive endocytosis mechanisms are involved in uptake of HIV-1 particles by monocyte-derived dendritic cells.Frontiers in immunology · 2024Article
- Loss of LncRNA DUXAP8 synergistically enhanced sorafenib induced ferroptosis in hepatocellular carcinoma via SLC7A11 de-palmitoylation.Clinical and translational medicine · 2023Article
- Differential CFTR-Interactome Proximity Labeling Procedures Identify Enrichment in Multiple SLC Transporters.International journal of molecular sciences · 2022Article
- Review
- Dynamic but discordant alterations in zDHHC5 expression and palmitoylation of its substrates in cardiac pathologies.Frontiers in physiology · 2022Article
- Mitochondrial respiration restricts Listeria monocytogenes infection by slowing down host cell receptor recycling.Cell reports · 2021Article
- Protein acylation by saturated very long chain fatty acids and endocytosis are involved in necroptosis.Cell chemical biology · 2021Article
- Mechanisms and functions of endocytosis in T cells.Cell communication and signaling : CCS · 2021Review
- FXYD proteins and sodium pump regulatory mechanisms.The Journal of general physiology · 2021Review
- Imaging the electrical activity of organelles in living cells.Communications biology · 2021Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Large Ca transients cause massive endocytosis (MEND) in BHK fibroblasts by nonclassical mechanisms. We present evidence that MEND depends on mitochondrial permeability transition pore (PTP) openings, followed by coenzyme A (CoA) release, acyl CoA synthesis, and membrane protein palmitoylation. MEND is blocked by inhibiting mitochondrial Ca uptake or PTP openings, depleting fatty acids, blocking acyl CoA synthesis, metabolizing CoA, or inhibiting palmitoylation. It is triggered by depolarizing mitochondria or promoting PTP openings. After mitochondrial MEND blockade, MEND is restored by cytoplasmic acyl CoA or CoA. MEND is blocked by siRNA knockdown of the plasmalemmal acyl transferase, DHHC5. When acyl CoA is abundant, transient H2O2 oxidative stress or PKC activation initiates MEND, but the immediate presence of H2O2 prevents MEND. The PTP inhibitor, NIM811, significantly increases plasmalemma in normally growing cells. Thus, the MEND pathway may contribute to constitutive as well as pathological plasmalemma turnover in dependence on mitochondrial stress signaling. DOI: http://dx.doi.org/10.7554/eLife.01293.001.
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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.