ArticleThe Journal of biological chemistry2010
Co-regulation of caveolar and Cdc42-dependent fluid phase endocytosis by phosphocaveolin-1.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 46 citations in OpenAlex.
- Entry of nanoparticles into cells and tissues: status and challenges.Beilstein journal of nanotechnology · 2024Article
- Functional genomics identify causal variant underlying the protective CTSH locus for Alzheimer's disease.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Article
- Epidermal growth factor regulates autophagy activity and endocytosis of yak cumulus cells in a concentration-dependent manner.Frontiers in veterinary science · 2022Article
- NELL2-cdc42 signaling regulates BAF complexes and Ewing sarcoma cell growth.Cell reports · 2021Article
- Review
- Caveolin1 Tyrosine-14 Phosphorylation: Role in Cellular Responsiveness to Mechanical Cues.The Journal of membrane biology · 2020Review
- The role of lipid species in membranes and cancer-related changes.Cancer metastasis reviews · 2020Review
- Lung Endothelial Transcytosis.Comprehensive Physiology · 2020Review
- Caveolin-1 Phosphorylation Is Essential for Axonal Growth of Human Neurons Derived From iPSCs.Frontiers in cellular neuroscience · 2019Article
- Clathrin-independent endocytosis: an increasing degree of complexity.Histochemistry and cell biology · 2018Review
- Endocytosis of tight junction proteins and the regulation of degradation and recycling.Annals of the New York Academy of Sciences · 2017Review
- Inter-domain tagging implicates caveolin-1 in insulin receptor trafficking and Erk signaling bias in pancreatic beta-cells.Molecular metabolism · 2016Article
- Molecular Determinants of the Cellular Entry of Asymmetric Peptide Dendrimers and Role of Caveolae.PloS one · 2016Article
- Caveolin-1 and CDC42 mediated endocytosis of silica-coated iron oxide nanoparticles in HeLa cells.Beilstein journal of nanotechnology · 2015Article
- Clathrin-independent pathways of endocytosis.Cold Spring Harbor perspectives in biology · 2014Article
- Endocytic crosstalk: cavins, caveolins, and caveolae regulate clathrin-independent endocytosis.PLoS biology · 2014Article
- Signaling mechanisms of glucose-induced F-actin remodeling in pancreatic islet β cells.Experimental & molecular medicine · 2013Review
- Prominin-2 expression increases protrusions, decreases caveolae and inhibits Cdc42 dependent fluid phase endocytosis.Biochemical and biophysical research communications · 2013Article
- Caveolae-dependent and -independent uptake of albumin in cultured rodent pulmonary endothelial cells.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Several clathrin-independent endocytosis mechanisms have been identified that can be distinguished by specific requirements for certain proteins, such as caveolin-1 (Cav1) and the Rho GTPases, RhoA and Cdc42, as well as by specific cargo. Some endocytic pathways may be co-regulated such that disruption of one pathway leads to the up-regulation of another; however, the underlying mechanisms for this are unclear. Cav1 has been reported to function as a guanine nucleotide dissociation inhibitor (GDI), which inhibits Cdc42 activation. We tested the hypothesis that Cav1 can regulate Cdc42-dependent, fluid phase endocytosis. We demonstrate that Cav1 overexpression decreases fluid phase endocytosis, whereas silencing of Cav1 enhances this pathway. Enhancement of Cav1 phosphorylation using a phosphatase inhibitor reduces Cdc42-regulated pinocytosis while stimulating caveolar endocytosis. Fluid phase endocytosis was inhibited by expression of a putative phosphomimetic mutant, Cav1-Y14E, but not by the phospho-deficient mutant, Cav1-Y14F. Overexpression of Cav2, or a Cav1 mutant in which the GDI region was altered to the corresponding sequence in Cav2, did not suppress fluid phase endocytosis. These results suggest that the Cav1 expression level and phosphorylation state regulates fluid phase endocytosis via the interaction between the Cav1 GDI region and Cdc42. These data define a novel molecular mechanism for co-regulation of two distinct clathrin-independent endocytic pathways.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.