Assembly and Turnover of Caveolae: What Do We Really Know?

被引:28
作者
Han, Bing [1 ]
Copeland, Courtney A. [1 ]
Tiwari, Ajit [1 ]
Kenworthy, Anne K. [1 ,2 ,3 ,4 ]
机构
[1] Vanderbilt Univ, Sch Med, Dept Mol Physiol & Biophys, Nashville, TN 37212 USA
[2] Vanderbilt Univ, Sch Med, Dept Cell & Dev Biol, Nashville, TN 37212 USA
[3] Vanderbilt Univ, Sch Med, Epithelial Biol Program, Nashville, TN 37212 USA
[4] Vanderbilt Univ, Chem & Phys Biol Program, 221 Kirkland Hall, Nashville, TN 37235 USA
来源
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY | 2016年 / 4卷
关键词
caveolae; caveolin-1; GFP; trafficking; degradation; breast cancer; pulmonary arterial hypertension; congenital generalized lipodystrophy; PLASMA-MEMBRANE; GOLGI-COMPLEX; P132L MUTATION; NULL MICE; PROTEIN; BREAST; INSIGHTS; MUTANT; CAVIN; OLIGOMERIZATION;
D O I
10.3389/fcell.2016.00068
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
In addition to containing highly dynamic nanoscale domains, the plasma membranes of many cell types are decorated with caveolae, flask shaped domains enriched in the structural protein caveolin-1 (Cav1). The importance of caveolae in numerous cellular functions and processes has become well-recognized, and recent years have seen dramatic advances in our understanding of how caveolae assemble and the mechanisms control the turnover of Cav1. At the same time, work from our lab and others have revealed that commonly utilized strategies such as overexpression and tagging of Cav1 have unexpectedly complex consequences on the trafficking and fate of Cav1. Here, we discuss the implications of these findings for current models of caveolae biogenesis and Cav1 turnover. In addition, we discuss how disease-associated mutants of Cav1 impact caveolae assembly and outline open questions in this still-emerging area.
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页数:7
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