ArticleMolecular biology of the cell2012
Caveolin targeting to late endosome/lysosomal membranes is induced by perturbations of lysosomal pH and cholesterol content.
Article in Molecular biology of the cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 71 citations in OpenAlex.
- Cholesterol Deficiency Directs Autophagy-Dependent Secretion of Extracellular Vesicles.Journal of extracellular vesicles · 2026Article
- Editorial: Mechanisms and novel therapeutic targets and approaches for mitochondrial dysfunction in neurological and cardiovascular diseases.Frontiers in physiology · 2026Article
- A Novel R140S γc Variant Alters Cellular Distribution, Reduces Surface Expression, and Impairs Cytokine Signaling in Atypical X-SCID.Journal of clinical immunology · 2025Article
- Mechanisms of autophagy-lysosome dysfunction in neurodegenerative diseases.Nature reviews. Molecular cell biology · 2024Review
- Caveolin-3 loss linked with the P104L LGMD-1C mutation modulates skeletal muscle mTORC1 signalling and cholesterol homeostasis.Journal of cachexia, sarcopenia and muscle · 2023Article
- Review
- A metabolic shift toward glycolysis enables cancer cells to maintain survival upon concomitant glutamine deprivation and V-ATPase inhibition.Frontiers in nutrition · 2023Article
- Glomerulopathic Light Chain-Mesangial Cell Interactions: Sortilin-Related Receptor (SORL1) and Signaling.Kidney international reports · 2021Article
- Article
- Receptor-type protein tyrosine phosphatase alpha (PTPα) mediates MMP14 localization and facilitates triple-negative breast cancer cell invasion.Molecular biology of the cell · 2021Article
- ECM deposition is driven by caveolin-1-dependent regulation of exosomal biogenesis and cargo sorting.The Journal of cell biology · 2020Article
- Cav-1 (Caveolin-1) Deficiency Increases Autophagy in the Endothelium and Attenuates Vascular Inflammation and Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Internalized FGF-2-Loaded Nanoparticles Increase Nuclear ERK1/2 Content and Result in Lung Cancer Cell Death.Nanomaterials (Basel, Switzerland) · 2020Article
- Microtubules in Polyomavirus Infection.Viruses · 2020Review
- Critical role of caveolin-1 in aflatoxin B1-induced hepatotoxicity via the regulation of oxidation and autophagy.Cell death & disease · 2020Article
- Cell Intrinsic and Extrinsic Mechanisms of Caveolin-1-Enhanced Metastasis.Biomolecules · 2019Review
- Linker length in fluorophore-cholesterol conjugates directs phase selectivity and cellular localisation in GUVs and live cells.RSC advances · 2019Article
- Caveolin-1 promotes invasion and metastasis by upregulating Pofut1 expression in mouse hepatocellular carcinoma.Cell death & disease · 2019Article
- Lysosome trafficking and signaling in health and neurodegenerative diseases.Neurobiology of disease · 2019Review
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Caveolin-1 is an integral membrane protein of plasma membrane caveolae. Here we report that caveolin-1 collects at the cytosolic surface of lysosomal membranes when cells are serum starved. This is due to an elevation of the intralysosomal pH, since ionophores and proton pump inhibitors that dissipate the lysosomal pH gradient also trapped caveolin-1 on late endosome/lysosomes. Accumulation is both saturable and reversible. At least a portion of the caveolin-1 goes to the plasma membrane upon reversal. Several studies suggest that caveolin-1 is involved in cholesterol transport within the cell. Strikingly, we find that blocking cholesterol export from lysosomes with progesterone or U18666A or treating cells with low concentrations of cyclodextrin also caused caveolin-1 to accumulate on late endosome/lysosomal membranes. Under these conditions, however, live-cell imaging shows cavicles actively docking with lysosomes, suggesting that these structures might be involved in delivering caveolin-1. Targeting of caveolin-1 to late endosome/lysosomes is not observed normally, and the degradation rate of caveolin-1 is not altered by any of these conditions, indicating that caveolin-1 accumulation is not a consequence of blocked degradation. We conclude that caveolin-1 normally traffics to and from the cytoplasmic surface of lysosomes during intracellular cholesterol trafficking.
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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.