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Correction: ERCC6L facilitates the progression of laryngeal squamous cell carcinoma by the binding of FOXM1 and KIF4A.
Cell Death Discov
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Department of Otorhinolaryngology Head and Neck Surgery, Peking University People's Hospital, Peking University, Xi Zhi Men South Street 11, Western District, Beijing, 100034, P.R. China.
Correction to: ERCC6L that is up-regulated in high grade of renal cell carcinoma enhances cell viability in vitro and promotes tumor growth in vivo potentially through modulating MAPK signalling pathway.
Cancer Gene Ther
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Department of Urology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning, 110042, China.
Bloom's syndrome and PICH helicases cooperate with topoisomerase IIα in centromere disjunction before anaphase.
PLoS One
September 2012
Institut Curie, Centre de Recherche, Centre Universitaire, Bât, Orsay, France.
Centromeres are specialized chromosome domains that control chromosome segregation during mitosis, but little is known about the mechanisms underlying the maintenance of their integrity. Centromeric ultrafine anaphase bridges are physiological DNA structures thought to contain unresolved DNA catenations between the centromeres separating during anaphase. BLM and PICH helicases colocalize at these ultrafine anaphase bridges and promote their resolution.
View Article and Find Full Text PDFUse of the novel Plk1 inhibitor ZK-thiazolidinone to elucidate functions of Plk1 in early and late stages of mitosis.
Mol Biol Cell
October 2007
Department of Cell Biology and Intracellular Protein Transport, Independent Junior Research Group, Max-Planck Institute of Biochemistry, Martinsried, 82152 Germany.
Polo-like kinase 1 (Plk1) is a key regulator of mitotic progression and cell division in eukaryotes. It is highly expressed in tumor cells and considered a potential target for cancer therapy. Here, we report the discovery and application of a novel potent small-molecule inhibitor of mammalian Plk1, ZK-Thiazolidinone (TAL).
View Article and Find Full Text PDFBLM is required for faithful chromosome segregation and its localization defines a class of ultrafine anaphase bridges.
EMBO J
July 2007
Cancer Research UK Laboratories, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, UK.
Mutations in BLM cause Bloom's syndrome, a disorder associated with cancer predisposition and chromosomal instability. We investigated whether BLM plays a role in ensuring the faithful chromosome segregation in human cells. We show that BLM-defective cells display a higher frequency of anaphase bridges and lagging chromatin than do isogenic corrected derivatives that eptopically express the BLM protein.
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