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Depletion of the nucleolar protein nucleostemin causes G1 cell cycle arrest via the p53 pathway
UMass Chan Affiliations
Department of Molecular Genetics and MicrobiologyDepartment of Biochemistry and Molecular Pharmacology
Program in Cell Dynamics
Document Type
Journal ArticlePublication Date
2007-05-15Keywords
ADP-Ribosylation FactorsCarrier Proteins
Cell Nucleolus
Down-Regulation
*G1 Phase
Hela Cells
Humans
Nuclear Proteins
Proto-Oncogene Proteins c-mdm2
Retinoblastoma ProteinTumor Suppressor Protein p53Up-RegulationLife SciencesMedicine and Health Sciences
Metadata
Show full item recordAbstract
Nucleostemin (NS) is a nucleolar protein expressed in adult and embryo-derived stem cells, transformed cell lines, and tumors. NS decreases when proliferating cells exit the cell cycle, but it is unknown how NS is controlled, and how it participates in cell growth regulation. Here, we show that NS is down-regulated by the tumor suppressor p14(ARF) and that NS knockdown elevates the level of tumor suppressor p53. NS knockdown led to G1 cell cycle arrest in p53-positive cells but not in cells in which p53 was genetically deficient or depleted by small interfering RNA knockdown. These results demonstrate that, in the cells investigated, the level of NS is regulated by p14(ARF) and the control of the G1/S transition by NS operates in a p53-dependent manner.Source
Mol Biol Cell. 2007 Jul;18(7):2630-5. Epub 2007 May 9. Link to article on publisher's siteDOI
10.1091/mbc.E07-03-0244Permanent Link to this Item
http://hdl.handle.net/20.500.14038/38457PubMed ID
17494866Related Resources
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