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Gene Review

CAV1  -  caveolin 1, caveolae protein, 22kDa

Sus scrofa

 
 
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Disease relevance of CAV1

  • Translocation of caveolin after exposure to oxidized LDL suggests that the localization of caveolin may be a valuable tool to study models of early atherogenesis [1].
 

High impact information on CAV1

  • Caveolae and caveolin-containing detergent-insoluble glycolipid-enriched rafts (DIG) have been implicated to function as plasma membrane microcompartments or domains for the preassembly of signaling complexes, keeping them in the basal inactive state [2].
  • This correlates well to increased tyrosine phosphorylation of caveolin and the insulin receptor substrate protein 1 (up to 6- and 15-fold), as well as elevated phosphatidylinositol-3' kinase activity and glucose transport (to up to 7- and 13-fold) [2].
  • These data suggest that in adipocytes a subset of signaling components is concentrated at caveolae-DIG via the interaction between their CBD and the CSD of caveolin [2].
  • Endothelial nitric-oxide synthase (eNOS) associates with caveolae and is directly regulated by the caveola protein, caveolin [3].
  • Cyclodextrin also depleted caveolae of cholesterol and caused eNOS and caveolin to translocate from caveolae [3].
 

Biological context of CAV1

 

Anatomical context of CAV1

 

Associations of CAV1 with chemical compounds

  • We demonstrated that A(1)R agonist N(6)-(R)-phenylisopropyl adenosine promotes the translocation of A(1)R into low-density gradient fractions containing caveolin [8].
  • Instead, we suggest that the ability of LacCer to confer detergent-insolubility on this GPI-anchored protein is dependent on the structure of the lipid molecule in its entirety, and that this glycosphingolipid may have an important role to play in the stabilization of lipid rafts, particularly the caveolin-free glycosphingolipid signalling domains [10].
  • CONCLUSION: The integrity of caveolin-1-containing membrane microdomains is prerequisite for arachidonic acid recruitment and EDHF signaling in porcine arteries [5].
  • Their lipid composition, 22% SM, 60% cholesterol, 11% phosphatidylethanolamine, 8% PC, <1% phosphatidylinositol, and coisolation with 5'-nucleotidase and caveolin-1 suggest that they are liquid-ordered membranes [11].
  • Treatment with methyl-beta-cyclodextrin--a cholesterol chelator--leads to a spreading of both caveolin and completely inactive Ca2+-ATPase toward high-density fractions [12].
 

Other interactions of CAV1

  • Depletion of caveolin-1 also significantly reduced the ouabain-induced accumulation of Na/K-ATPase alpha-1 subunit, EGFR, Src, and MAPKs in clathrin-coat vesicles, as well as early and late endosomes [4].
  • NOS-3, HSP90, and caveolin-1 levels were similar in hypoxic and control PAs [13].
  • During mass transfer studies using alpha TocH-enriched HDL, approximately 50% of cellular alpha TocH was recovered with the bulk of cellular caveolin-1 and SR-BI [9].
  • We show that the GPI-anchored protein membrane dipeptidase is localized in detergent-insoluble lipid rafts isolated from porcine kidney microvillar membranes, and that these rafts, which lack caveolin, are enriched not only in sphingomyelin and cholesterol, but also in the glycosphingolipid lactosylceramide (LacCer) [10].
  • Immunoblot and immunohistochemistry results indicate the following: 1) LAD endothelial NOS protein content was similar among groups; 2) HF decreased LAD superoxide dismutase (SOD) but increased caveolin-1 content; and 3) Ex increased SOD content of HF LADs [14].
 

Analytical, diagnostic and therapeutic context of CAV1

References

  1. Localization of caveolin 1 in aortic valve endothelial cells using antigen retrieval. Rajamannan, N.M., Springett, M.J., Pederson, L.G., Carmichael, S.W. J. Histochem. Cytochem. (2002) [Pubmed]
  2. Redistribution of glycolipid raft domain components induces insulin-mimetic signaling in rat adipocytes. Müller, G., Jung, C., Wied, S., Welte, S., Jordan, H., Frick, W. Mol. Cell. Biol. (2001) [Pubmed]
  3. Oxidized low density lipoprotein displaces endothelial nitric-oxide synthase (eNOS) from plasmalemmal caveolae and impairs eNOS activation. Blair, A., Shaul, P.W., Yuhanna, I.S., Conrad, P.A., Smart, E.J. J. Biol. Chem. (1999) [Pubmed]
  4. Ouabain-induced endocytosis of the plasmalemmal Na/K-ATPase in LLC-PK1 cells requires caveolin-1. Liu, J., Liang, M., Liu, L., Malhotra, D., Xie, Z., Shapiro, J.I. Kidney Int. (2005) [Pubmed]
  5. Cholesterol- and caveolin-rich membrane domains are essential for phospholipase A2-dependent EDHF formation. Graziani, A., Bricko, V., Carmignani, M., Graier, W.F., Groschner, K. Cardiovasc. Res. (2004) [Pubmed]
  6. Metabolic organization in vascular smooth muscle: distribution and localization of caveolin-1 and phosphofructokinase. Vallejo, J., Hardin, C.D. Am. J. Physiol., Cell Physiol. (2004) [Pubmed]
  7. A caveolar complex between the cationic amino acid transporter 1 and endothelial nitric-oxide synthase may explain the "arginine paradox". McDonald, K.K., Zharikov, S., Block, E.R., Kilberg, M.S. J. Biol. Chem. (1997) [Pubmed]
  8. Involvement of caveolin in ligand-induced recruitment and internalization of A(1) adenosine receptor and adenosine deaminase in an epithelial cell line. Ginés, S., Ciruela, F., Burgueño, J., Casadó, V., Canela, E.I., Mallol, J., Lluís, C., Franco, R. Mol. Pharmacol. (2001) [Pubmed]
  9. Uptake and transport of high-density lipoprotein (HDL) and HDL-associated alpha-tocopherol by an in vitro blood-brain barrier model. Balazs, Z., Panzenboeck, U., Hammer, A., Sovic, A., Quehenberger, O., Malle, E., Sattler, W. J. Neurochem. (2004) [Pubmed]
  10. Differential effects of glycosphingolipids on the detergent-insolubility of the glycosylphosphatidylinositol-anchored membrane dipeptidase. Parkin, E.T., Turner, A.J., Hooper, N.M. Biochem. J. (2001) [Pubmed]
  11. Smooth muscle raft-like membranes. Baron, C.B., Coburn, R.F. J. Lipid Res. (2004) [Pubmed]
  12. The plasma membrane Ca2+ pump from proximal kidney tubules is exclusively localized and active in caveolae. Tortelote, G.G., Valverde, R.H., Lemos, T., Guilherme, A., Einicker-Lamas, M., Vieyra, A. FEBS Lett. (2004) [Pubmed]
  13. Impaired NO signaling in small pulmonary arteries of chronically hypoxic newborn piglets. Fike, C.D., Aschner, J.L., Zhang, Y., Kaplowitz, M.R. Am. J. Physiol. Lung Cell Mol. Physiol. (2004) [Pubmed]
  14. Exercise preserves endothelium-dependent relaxation in coronary arteries of hypercholesterolemic male pigs. Thompson, M.A., Henderson, K.K., Woodman, C.R., Turk, J.R., Rush, J.W., Price, E., Laughlin, M.H. J. Appl. Physiol. (2004) [Pubmed]
  15. Loss of caveolin expression in type I pneumocytes as an indicator of subcellular alterations during lung fibrogenesis. Kasper, M., Reimann, T., Hempel, U., Wenzel, K.W., Bierhaus, A., Schuh, D., Dimmer, V., Haroske, G., Müller, M. Histochem. Cell Biol. (1998) [Pubmed]
  16. Identification of caveolae and their signature proteins caveolin 1 and 2 in the lens. Lo, W.K., Zhou, C.J., Reddan, J. Exp. Eye Res. (2004) [Pubmed]
 
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