| pubmed-article:15713235 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15713235 | lifeskim:mentions | umls-concept:C0242608 | lld:lifeskim |
| pubmed-article:15713235 | lifeskim:mentions | umls-concept:C0010813 | lld:lifeskim |
| pubmed-article:15713235 | lifeskim:mentions | umls-concept:C1512977 | lld:lifeskim |
| pubmed-article:15713235 | lifeskim:mentions | umls-concept:C0237753 | lld:lifeskim |
| pubmed-article:15713235 | lifeskim:mentions | umls-concept:C0231174 | lld:lifeskim |
| pubmed-article:15713235 | lifeskim:mentions | umls-concept:C0333694 | lld:lifeskim |
| pubmed-article:15713235 | lifeskim:mentions | umls-concept:C1155874 | lld:lifeskim |
| pubmed-article:15713235 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:15713235 | pubmed:dateCreated | 2005-3-14 | lld:pubmed |
| pubmed-article:15713235 | pubmed:abstractText | Mammalian cells have been reported to have a p53-dependent tetraploidy checkpoint that blocks cell cycle progression in G1 in response to failure of cell division. In most cases where the tetraploidy checkpoint has been observed cell division was perturbed by anti-cytoskeleton drug treatments. However, other evidence argues against the existence of a tetraploidy checkpoint. Cells that have failed to divide differ from normal cells in having two nuclei, two centrosomes, a decreased surface to volume ratio, and having undergone an abortive cytokinesis. We tested each of these to determine which, if any, cause a G1 cell cycle arrest. | lld:pubmed |
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| pubmed-article:15713235 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15713235 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15713235 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15713235 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15713235 | pubmed:issn | 1471-2121 | lld:pubmed |
| pubmed-article:15713235 | pubmed:author | pubmed-author:StearnsTimT | lld:pubmed |
| pubmed-article:15713235 | pubmed:author | pubmed-author:WongConnieC | lld:pubmed |
| pubmed-article:15713235 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:15713235 | pubmed:volume | 6 | lld:pubmed |
| pubmed-article:15713235 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15713235 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15713235 | pubmed:pagination | 6 | lld:pubmed |
| pubmed-article:15713235 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
| pubmed-article:15713235 | pubmed:meshHeading | pubmed-meshheading:15713235... | lld:pubmed |
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| pubmed-article:15713235 | pubmed:meshHeading | pubmed-meshheading:15713235... | lld:pubmed |
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| pubmed-article:15713235 | pubmed:meshHeading | pubmed-meshheading:15713235... | lld:pubmed |
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| pubmed-article:15713235 | pubmed:meshHeading | pubmed-meshheading:15713235... | lld:pubmed |
| pubmed-article:15713235 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15713235 | pubmed:articleTitle | Mammalian cells lack checkpoints for tetraploidy, aberrant centrosome number, and cytokinesis failure. | lld:pubmed |
| pubmed-article:15713235 | pubmed:affiliation | Department of Biological Sciences, Stanford University, Stanford, CA 94305, USA. conniewg@stanford.edu | lld:pubmed |
| pubmed-article:15713235 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15713235 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15713235 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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