Identification of the nuclear localization signal of p21cip1 and consequences of its mutation on cell proliferation

FEBS Letters

Rahn, Hans-Peter¹  Agell, Neus¹  Dı́az, Carmen¹  Canela, Núria¹  Rodrı́guez-Vilarrupla, Aina¹  Bachs, Oriol¹ 

[1] Departament de Biologia Cellular i Anatomia Patològica, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Facultat de Medicina, Universitat de Barcelona, C/Casanova, 143, 08036 Barcelona, Spain

关键词: p21cip1;    p21;    CKI;    Cell cycle;    Nuclear localization signal;    Nuclear transport;    p21;    p21cip1;    cdk;    cyclin-dependent kinase;    NLS;    nuclear localization signal;    GFP;    green fluorescent protein;   

DOI  :  10.1016/S0014-5793(02)03549-4

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Overexpression of p21^cip1 induces cell cycle arrest. Although this ability has been correlated with its nuclear localization, the evidence is not conclusive. The mutants that were used to inhibit its nuclear translocation could no longer bind to several proteins known to interact with the last 25 amino acids of p21^cip1. Here we used point mutation analysis and fusion of the proteins to DsRed to identify which amino acids are essential for the nuclear localization of p21^cip1. We conclude that amino acids RKR^140–142 are essential for nuclear translocation of p21^cip1. While wild-type DsRed-p21 induces cell cycle arrest in 95% of transfected cells, overexpression of cytoplasmatic p21AAA^140–142 arrested only 20% of transfected cells. We conclude that cytoplasmatic p21, with no deletion in the C-terminal region, had a much lower capacity to arrest the cell cycle.

【 授权许可】

Unknown