pubmed-article:9115433 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9115433 | lifeskim:mentions | umls-concept:C0007709 | lld:lifeskim |
pubmed-article:9115433 | lifeskim:mentions | umls-concept:C0008545 | lld:lifeskim |
pubmed-article:9115433 | lifeskim:mentions | umls-concept:C1155874 | lld:lifeskim |
pubmed-article:9115433 | lifeskim:mentions | umls-concept:C0597767 | lld:lifeskim |
pubmed-article:9115433 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:9115433 | pubmed:dateCreated | 1997-7-10 | lld:pubmed |
pubmed-article:9115433 | pubmed:abstractText | An emerging view is that the formation of active centromeres is modulated in an epigenetic manner reflecting the association of centromeres with heterochromatin. Support for this comes from studies on fission yeast centromeres, the properties of human neocentromeres and dicentric chromosomes, and analyses of Drosophila minichromosome deletion derivatives. A link has been established between tension across kinetochores and the phosphorylation status of kinetochore components. Vertebrate homologues of yeast MAD2 have recently been isolated and localized to kinetochores, indicating that components of the spindle integrity checkpoint are conserved. The linkage between sister chromatids is only dissolved at anaphase during mitotic and meiotic divisions. Phenotypic and localization data combined with their pattern of rapid degradation at anaphase have implicated several yeast and Drosophila proteins in aspects of sister chromatid cohesion. | lld:pubmed |
pubmed-article:9115433 | pubmed:language | eng | lld:pubmed |
pubmed-article:9115433 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9115433 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:9115433 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9115433 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9115433 | pubmed:month | Apr | lld:pubmed |
pubmed-article:9115433 | pubmed:issn | 0959-437X | lld:pubmed |
pubmed-article:9115433 | pubmed:author | pubmed-author:AllshireR CRC | lld:pubmed |
pubmed-article:9115433 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9115433 | pubmed:volume | 7 | lld:pubmed |
pubmed-article:9115433 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9115433 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9115433 | pubmed:pagination | 264-73 | lld:pubmed |
pubmed-article:9115433 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
pubmed-article:9115433 | pubmed:meshHeading | pubmed-meshheading:9115433-... | lld:pubmed |
pubmed-article:9115433 | pubmed:meshHeading | pubmed-meshheading:9115433-... | lld:pubmed |
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pubmed-article:9115433 | pubmed:meshHeading | pubmed-meshheading:9115433-... | lld:pubmed |
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pubmed-article:9115433 | pubmed:meshHeading | pubmed-meshheading:9115433-... | lld:pubmed |
pubmed-article:9115433 | pubmed:year | 1997 | lld:pubmed |
pubmed-article:9115433 | pubmed:articleTitle | Centromeres, checkpoints and chromatid cohesion. | lld:pubmed |
pubmed-article:9115433 | pubmed:affiliation | MRC Human Genetics Unit, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, UK. robin@hgu.mrc.ac.uk | lld:pubmed |
pubmed-article:9115433 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9115433 | pubmed:publicationType | Review | lld:pubmed |
pubmed-article:9115433 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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