{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T13:11:14Z","timestamp":1790514674532,"version":"4.1.0"},"reference-count":43,"publisher":"National Academy of Sciences","issue":"8","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2007,2,20]]},"abstract":"<jats:p>\n                    Numerical and\/or structural centrosome abnormalities have been correlated with most solid tumors and hematological malignancies. Tumorigenesis also is linked to defects in the mitotic or spindle assembly checkpoint, a key control mechanism that ensures accurate segregation of chromosomes during mitosis. We have reported that targeted disruption of the\n                    <jats:italic>Dido<\/jats:italic>\n                    gene causes a transplantable myelodysplastic\/myeloproliferative disease in mice. Here, we report that Dido3, the largest splice variant of the\n                    <jats:italic>Dido<\/jats:italic>\n                    gene, is a centrosome-associated protein whose disruption leads to supernumerary centrosomes, failure to maintain cellular mitotic arrest, and early degradation of the mitotic checkpoint protein BubR1. These aberrations result in enhanced aneuploidy in the\n                    <jats:italic>Dido<\/jats:italic>\n                    mutant cells.\n                    <jats:italic>Dido<\/jats:italic>\n                    gene malfunction thus is reported to be part of an impaired signaling cascade that results in a defective mitotic checkpoint, leading to chromosome instability.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0611132104","type":"journal-article","created":{"date-parts":[[2007,2,13]],"date-time":"2007-02-13T21:48:54Z","timestamp":1171403334000},"page":"2691-2696","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":43,"title":["<i>Dido<\/i>\n                    disruption leads to centrosome amplification and mitotic checkpoint defects compromising chromosome stability"],"prefix":"10.1073","volume":"104","author":[{"given":"Varvara","family":"Trachana","sequence":"first","affiliation":[{"name":"Department of Immunology and Oncology, Centro Nacional de Biotecnolog\u00eda\/Consejo Superior de Investigaciones Cientificas, Darwin 3, Campus de Cantoblanco, E-28049 Madrid, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karel H. M.","family":"van Wely","sequence":"additional","affiliation":[{"name":"Department of Immunology and Oncology, Centro Nacional de Biotecnolog\u00eda\/Consejo Superior de Investigaciones Cientificas, Darwin 3, Campus de Cantoblanco, E-28049 Madrid, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Astrid Alonso","family":"Guerrero","sequence":"additional","affiliation":[{"name":"Department of Immunology and Oncology, Centro Nacional de Biotecnolog\u00eda\/Consejo Superior de Investigaciones Cientificas, Darwin 3, Campus de Cantoblanco, E-28049 Madrid, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Agnes","family":"F\u00fctterer","sequence":"additional","affiliation":[{"name":"Department of Immunology and Oncology, Centro Nacional de Biotecnolog\u00eda\/Consejo Superior de Investigaciones Cientificas, Darwin 3, Campus de Cantoblanco, E-28049 Madrid, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carlos","family":"Mart\u00ednez-A","sequence":"additional","affiliation":[{"name":"Department of Immunology and Oncology, Centro Nacional de Biotecnolog\u00eda\/Consejo Superior de Investigaciones Cientificas, Darwin 3, Campus de Cantoblanco, E-28049 Madrid, 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