Document Detail


Accumulation of multiple forms of lamin A with down-regulation of FACE-1 suppresses growth in senescent human cells.
MedLine Citation:
PMID:  17352743     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
5-Bromodeoxyuridine (BrdU) clearly induces a senescence-like phenomenon in every cell type. Proteome analysis revealed that lamin A and C were most highly increased in the nuclei of HeLa cells upon addition of BrdU. Immunoblot analysis also revealed marked accumulation of nuclear prelamin A. Consistently, farnesylated-proteins converting enzyme 1 (FACE-1) was markedly down-regulated in the same cells. Similar phenomena were also observed in normal human fibroblasts undergoing replicative senescence. Immunochemical analysis confirmed the above results. Lamin A is a major component of lamina and responsible for several genetic diseases. Thus, we ectopically expressed a wild-type, a mature type and a premature type of lamin in HeLa cells. All of these forms similarly inhibited colony formation and delayed cell cycle progression mainly through G2 phase. These results suggest that a change in the amount of lamin A, rather than appearance of its truncated form, is responsible for growth retardation in affected cells.
Authors:
Ryo Ukekawa; Kensuke Miki; Michihiko Fujii; Hisashi Hirano; Dai Ayusawa
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Genes to cells : devoted to molecular & cellular mechanisms     Volume:  12     ISSN:  1356-9597     ISO Abbreviation:  Genes Cells     Publication Date:  2007 Mar 
Date Detail:
Created Date:  2007-03-13     Completed Date:  2007-05-03     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9607379     Medline TA:  Genes Cells     Country:  England    
Other Details:
Languages:  eng     Pagination:  397-406     Citation Subset:  IM    
Affiliation:
Department of Biochemistry, Kihara Institute for Biological Research, Yokohama City University, Maioka-cho 641-12, Yokohama 244-0813, Japan.
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MeSH Terms
Descriptor/Qualifier:
Base Sequence
Cell Aging
Cell Line
Cell Nucleus / metabolism
DNA Primers / genetics
Down-Regulation
Hela Cells
Humans
Lamin Type A / genetics,  metabolism*
Lipoproteins / genetics*
Membrane Proteins / genetics*
Metalloendopeptidases
Metalloproteases / genetics*
Nuclear Proteins / genetics,  metabolism
Protein Precursors / genetics,  metabolism
RNA, Messenger / genetics,  metabolism
RNA, Small Interfering / genetics
Chemical
Reg. No./Substance:
0/DNA Primers; 0/LMNA protein, human; 0/Lamin Type A; 0/Lipoproteins; 0/Membrane Proteins; 0/Nuclear Proteins; 0/Protein Precursors; 0/RNA, Messenger; 0/RNA, Small Interfering; 0/prelamin A; EC 3.4.-/Metalloproteases; EC 3.4.24.-/Metalloendopeptidases; EC 3.4.24.84/ZMPSTE24 protein, human

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


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