ArticleMolecular biology of the cell2009
Caveolin-2 is required for apical lipid trafficking and suppresses basolateral recycling defects in the intestine of Caenorhabditis elegans.
Article in Molecular biology of the cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Effect ofNAM journal · 2025Article
- Extracellular vesicle transfer of miR-1 to adipose tissue modifies lipolytic pathways following resistance exercise.JCI insight · 2024Article
- Mobilization of cholesterol induces the transition from quiescence to growth in Caenorhabditis elegans through steroid hormone and mTOR signaling.Communications biology · 2024Article
- EGFR signal transduction is downregulated in C. elegans vulval precursor cells during dauer diapause.Development (Cambridge, England) · 2022Article
- AP2M1 Supports TGF-β Signals to Promote Collagen Expression by Inhibiting Caveolin Expression.International journal of molecular sciences · 2021Article
- Article
- Modulation of caveolae by insulin/IGF-1 signaling regulates aging ofEMBO reports · 2018Article
- Article
- Nerve Growth Factor Signaling from Membrane Microdomains to the Nucleus: Differential Regulation by Caveolins.International journal of molecular sciences · 2017Article
- Intestinal epithelial cell caveolin 1 regulates fatty acid and lipoprotein cholesterol plasma levels.Disease models & mechanisms · 2017Article
- Exposure to dietary lipid leads to rapid production of cytosolic lipid droplets near the brush border membrane.Nutrition & metabolism · 2016Article
- Dynamic caveolae exclude bulk membrane proteins and are required for sorting of excess glycosphingolipids.Nature communications · 2015Article
- Loss of the Sec1/Munc18-family proteins VPS-33.2 and VPS-33.1 bypasses a block in endosome maturation in Caenorhabditis elegans.Molecular biology of the cell · 2014Article
- Functional characterization of thioredoxin 3 (TRX-3), a Caenorhabditis elegans intestine-specific thioredoxin.Free radical biology & medicine · 2014Article
- Intestinal caveolin-1 is important for dietary fatty acid absorption.Biochimica et biophysica acta · 2013Article
- Caveolin-2 is a negative regulator of anti-proliferative function and signaling of transforming growth factor-β in endothelial cells.American journal of physiology. Cell physiology · 2011Article
- Novel insights into the role of caveolin-2 in cell- and tissue-specific signaling and function.Biochemistry research international · 2011Article
- A monoclonal antibody toolkit for C. elegans.PloS one · 2010Article
- Endothelial cells isolated from caveolin-2 knockout mice display higher proliferation rate and cell cycle progression relative to their wild-type counterparts.American journal of physiology. Cell physiology · 2010Article
- Overexpression of caveolins in Caenorhabditis elegans induces changes in egg-laying and fecundity.Communicative & integrative biology · 2009Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Caveolins are plasma membrane-associated proteins that colocalize with, and stabilize caveolae. Their functions remain unclear although they are known to be involved in specific events in cell signaling and endocytosis. Caenorhabditis elegans encodes two caveolin genes, cav-1 and cav-2. We show that cav-2 is expressed in the intestine where it is localized to the apical membrane and in intracellular bodies. Using the styryl dye FM4-64 and BODIPY-labeled lactosylceramide, we show that the intestinal cells of cav-2 animals are defective in the apical uptake of lipid markers. These results suggest parallels with the function of caveolins in lipid homeostasis in mammals. We also show that CAV-2 depletion suppresses the abnormal accumulation of vacuoles that result from defective basolateral recycling in rme-1 and rab-10 mutants. Analysis of fluorescent markers of basolateral endocytosis and recycling suggest that endocytosis is normal in cav-2 mutants and thus, that the suppression of basolateral recycling defects in cav-2 mutants is due to changes in intracellular trafficking pathways. Finally, cav-2 mutants also have abnormal trafficking of yolk proteins. Taken together, these data indicate that caveolin-2 is an integral component of the trafficking network in the intestinal cells of C. elegans.
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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.