p57KIP2: "Kip"ing the Cell under Control

被引：124
作者：
Pateras, Ioannis S. [1 ]
Apostolopoulou, Kalliopi [1 ]
Niforou, Katerina [1 ]
Kotsinas, Athanassios [1 ]
Gorgoulis, Vassilis G. [1 ]
机构：
[1] Univ Athens, Mol Carcinogenesis Grp, Lab Histol Embryol, Sch Med, GR-10679 Athens, Greece
来源：
MOLECULAR CANCER RESEARCH | 2009年 / 7卷 / 12期
关键词：
BECKWITH-WIEDEMANN-SYNDROME; DEPENDENT-KINASE INHIBITOR; GESTATIONAL TROPHOBLASTIC DISEASE; ACUTE LYMPHOCYTIC-LEUKEMIA; ABERRANT DNA METHYLATION; TUMOR-SUPPRESSOR GENE; HISTONE-H3; LYSINE-9; METHYLATION; PREECLAMPSIA-LIKE SYMPTOMS; EPITHELIAL OVARIAN-TUMORS; MOUSE DISTAL CHROMOSOME-7;
D O I：
10.1158/1541-7786.MCR-09-0317
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
p57(KIP2) is an imprinted gene located at the chromosomal locus 11p15.5. It is a cyclin-dependent kinase inhibitor belonging to the CIP/KIP family, which includes additionally p21(CIP1/WAF1) and p27(KIP1). It is the least studied CIP/KIP member and has a unique role in embryogenesis. p57(KIP2) regulates the cell cycle, although novel functions have been attributed to this protein including cytoskeletal organization. Molecular analysis of animal models and patients with Beckwith-Wiedemann Syndrome have shown its nodal implication in the pathogenesis of this syndrome. p57(KIP2) is frequently down-regulated in many common human malignancies through several mechanisms, denoting its anti-oncogenic function. This review is a thorough analysis of data available on p57(KIP2), in relation to p21(CIP1/WAF1) and p27(KIP1), on gene and protein structure, its transcriptional and translational regulation, and its role in human physiology and pathology, focusing on cancer development. (Mol Cancer Res 2009;7(12):1902-19)
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收藏
页码：1902 / 1919
页数：18
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