[Effect of inactivating the p33ING1 tumor suppressor on the function of cell cycle 'checkpoints' and genome stability]
| Autor: | Na, Turovets, Ls, Agapova, Pb, Kopnin, Nm, Tulina, Peter Chumakov, Bp, Kopnin |
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| Předmět: |
DNA Replication
Phosphonoacetic Acid Aspartic Acid Genome Tumor Suppressor Proteins Cell Cycle Demecolcine Intracellular Signaling Peptides and Proteins Nuclear Proteins Proteins Cell Cycle Proteins Rats DNA-Binding Proteins Polyploidy Transduction Genetic Ethyl Methanesulfonate Animals Humans Genes Tumor Suppressor Sister Chromatid Exchange Inhibitor of Growth Protein 1 |
| Zdroj: | Europe PubMed Central |
| Popis: | Novel candidate tumor suppressor p33ING1 is known to regulate activity of the p53 protein. The effect of p33ING1 inactivation on the functioning of the cell cycle "checkpoints" and the frequency of chromosomal aberrations was examined. Transduction of the p33-GSEas genetic suppressor element, known to reduce the p53 activity, into p53-positive rat and human cells resulted in: (1) partial abolishment of ethylmetansulphonate- or colcemid-induced arrest of the G1-to-S transition in the G0-synchronized cultures; (2) abolishment of the block in the S phase by the DNA synthesis inhibitor, N-phosphonacetil-L-aspartate (PALA); (3) an increase of the number of spontaneous chromosomal breaks and sister-chromatid exchanges; (4) increased frequency of colchicine-induced polyploidy. Similar effects were observed upon transduction of the p53-GSE22 genetic suppressor element, known to reduce p53 transcriptional activity. Presumably, the effect of p33ING1 inactivation on the cell cycle checkpoints and genetic stability is associated with a decrease in p53 activity. |
| Databáze: | OpenAIRE |
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