Document Detail


Identification of the nuclear localization signal of p21(cip1) and consequences of its mutation on cell proliferation.
MedLine Citation:
PMID:  12417334     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Aina Rodríguez-Vilarrupla; Carmen Díaz; Núria Canela; Hans Peter Rahn; Oriol Bachs; Neus Agell
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  FEBS letters     Volume:  531     ISSN:  0014-5793     ISO Abbreviation:  FEBS Lett.     Publication Date:  2002 Nov 
Date Detail:
Created Date:  2002-11-05     Completed Date:  2002-12-09     Revised Date:  2006-11-20    
Medline Journal Info:
Nlm Unique ID:  0155157     Medline TA:  FEBS Lett     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  319-23     Citation Subset:  IM    
Affiliation:
Departament de Biologia Cellular i Anatomia Patològica, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Facultat de Medicina, Universitat de Barcelona, C/Casanova, Barcelona, Spain.
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MeSH Terms
Descriptor/Qualifier:
3T3 Cells
Active Transport, Cell Nucleus
Amino Acid Sequence
Animals
COS Cells
Calmodulin / metabolism
Cell Cycle
Cell Division
Cell Nucleus / metabolism*
Chromosomal Proteins, Non-Histone
Cyclin-Dependent Kinase Inhibitor p21
Cyclins / chemistry*,  genetics,  physiology
DNA Mutational Analysis
Mice
Molecular Sequence Data
Nuclear Localization Signals
Point Mutation
Proliferating Cell Nuclear Antigen / metabolism
Proteins / metabolism
Recombinant Fusion Proteins / metabolism
Transcription Factors
Chemical
Reg. No./Substance:
0/Calmodulin; 0/Cdkn1a protein, mouse; 0/Chromosomal Proteins, Non-Histone; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Cyclins; 0/Nuclear Localization Signals; 0/Proliferating Cell Nuclear Antigen; 0/Proteins; 0/Recombinant Fusion Proteins; 0/Transcription Factors

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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