| Accumulation of multiple forms of lamin A with down-regulation of FACE-1 suppresses growth in senescent human cells. | |
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MedLine Citation:
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PMID: 17352743 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Ryo Ukekawa; Kensuke Miki; Michihiko Fujii; Hisashi Hirano; Dai Ayusawa |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Genes to cells : devoted to molecular & cellular mechanisms Volume: 12 ISSN: 1356-9597 ISO Abbreviation: Genes Cells Publication Date: 2007 Mar |
Date Detail:
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Created Date: 2007-03-13 Completed Date: 2007-05-03 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 9607379 Medline TA: Genes Cells Country: England |
Other Details:
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Languages: eng Pagination: 397-406 Citation Subset: IM |
Affiliation:
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Department of Biochemistry, Kihara Institute for Biological Research, Yokohama City University, Maioka-cho 641-12, Yokohama 244-0813, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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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 |
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