| http://purl.uniprot.org/citations/15930286 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15930286 | http://www.w3.org/2000/01/rdf-schema#comment | "Chromosomal instability (CIN) has been recognized as a hallmark of human cancer and is caused by continuous chromosome missegregation during mitosis. Proper chromosome segregation requires a physical connection between spindle microtubules and centromeric DNA and this attachment occurs at proteinaceous structures called kinetochore. Several centromere proteins such as CENP-A and CENP-H are the fundamental components of the human active kinetochore, and inappropriate expression of the centromere proteins could be a major cause of CIN. We have previously shown that CENP-A was overexpressed in primary human colorectal cancer. In this study, we show that CENP-H was also up-regulated in all of 15 primary human colorectal cancer tissues as well as in CIN tumor cell lines. Surprisingly, transient transfection of CENP-H expression plasmid into the diploid cell line HCT116 remarkably induced aneupoidy. Moreover, CENP-H stable transfectant of mouse embryonic fibroblast/3T3 cell lines showed aberrant interphase micronuclei, characteristic of chromosome missegregation. In these CENP-H overexpressed cells, CENP-H completely disappeared from the centromere of mitotic chromosomes, which might be the cause of the chromosome segregation defect. These results suggest that the aberrant expression and localization of a kinetochore protein CENP-H plays an important role in the aneuploidy frequently observed in colorectal cancers."xsd:string |
| http://purl.uniprot.org/citations/15930286 | http://purl.org/dc/terms/identifier | "doi:10.1158/0008-5472.can-04-3613"xsd:string |
| http://purl.uniprot.org/citations/15930286 | http://purl.uniprot.org/core/author | "Matsushita K."xsd:string |
| http://purl.uniprot.org/citations/15930286 | http://purl.uniprot.org/core/author | "Ishibashi M."xsd:string |
| http://purl.uniprot.org/citations/15930286 | http://purl.uniprot.org/core/author | "Shimada H."xsd:string |
| http://purl.uniprot.org/citations/15930286 | http://purl.uniprot.org/core/author | "Yoda K."xsd:string |
| http://purl.uniprot.org/citations/15930286 | http://purl.uniprot.org/core/author | "Ochiai T."xsd:string |
| http://purl.uniprot.org/citations/15930286 | http://purl.uniprot.org/core/author | "Nomura F."xsd:string |
| http://purl.uniprot.org/citations/15930286 | http://purl.uniprot.org/core/author | "Tomonaga T."xsd:string |
| http://purl.uniprot.org/citations/15930286 | http://purl.uniprot.org/core/author | "Nezu M."xsd:string |
| http://purl.uniprot.org/citations/15930286 | http://purl.uniprot.org/core/date | "2005"xsd:gYear |
| http://purl.uniprot.org/citations/15930286 | http://purl.uniprot.org/core/name | "Cancer Res"xsd:string |
| http://purl.uniprot.org/citations/15930286 | http://purl.uniprot.org/core/pages | "4683-4689"xsd:string |
| http://purl.uniprot.org/citations/15930286 | http://purl.uniprot.org/core/title | "Centromere protein H is up-regulated in primary human colorectal cancer and its overexpression induces aneuploidy."xsd:string |
| http://purl.uniprot.org/citations/15930286 | http://purl.uniprot.org/core/volume | "65"xsd:string |
| http://purl.uniprot.org/citations/15930286 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/15930286 |
| http://purl.uniprot.org/citations/15930286 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/15930286 |
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