Regulation of the endothelial cell cycle by the ubiquitin-proteasome system

被引:45
作者
Fasanaro, Pasquale [1 ]
Capogrossi, Maurizio C. [1 ]
Martelli, Fabio [1 ]
机构
[1] Ist Dermopat Immacolata IRCCS, Lab Patol Vascolare, Rome, Italy
关键词
Cell cycle; Endothelium; Oxidative stress; Proteasome; Ubiquitin; NF-KAPPA-B; ANAPHASE-PROMOTING COMPLEX/CYCLOSOME; OXIDATIVE STRESS; DEUBIQUITINATING ENZYME; BETA-TRCP; S-PHASE; DIFFERENTIAL REGULATION; MEDIATED DESTRUCTION; CATALYTIC MECHANISM; PROTEIN-DEGRADATION;
D O I
10.1093/cvr/cvp244
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Degradation of poly-ubiquitinated proteins by the 26S-proteasome complex represents a crucial quantitative control mechanism. The ubiquitin-proteasome system (UPS) plays a pivotal role in the complex molecular network regulating the progression both between and within each cell-cycle phase. Two major complexes are involved: the SKP1-CUL1-F-box-protein complex (SCF) and the anaphase-promoting complex/cyclosome (APC/C). Notwithstanding structural similarities, SCF and APC/C display different cellular functions and mechanisms of action. SCF modulates all cell-cycle stages and plays a prominent role at G1/S transition mainly through three regulatory subunits: Skp2, Fbw7, and beta-TRCP. APC/C, regulated by Cdc20 or Cdh1 subunits, has a crucial role in mitosis. In this review, we will describe how the endothelial cell cycle is regulated by the UPS. We will illustrate the principal SCF- and APC/C-dependent molecular mechanisms that modulate cell growth, allowing a unidirectional cell-cycle progression. Then, we will focus our attention on UPS modulation by oxidative stress, a pathogenic stimulus that causes endothelial dysfunction and is involved in numerous cardiovascular diseases.
引用
收藏
页码:272 / 280
页数:9
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