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KIF-2C expression in tumor tissues may serve as an independent prognostic marker for male, but not female, patients with operable esophageal squamous cell carcinomas.
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these findings demonstrate that p53 can repress MCAK promoter activity indirectly via down-regulation of Sp1 expression level, and suggest that MCAK elevation in human tumor cells might be due to p53 mutation
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Results show that three residues (K524, E525 and R528), which are located in the C-terminal half of the a4-helix, play a crucial role in the ability of MCAK to distinguish between the microtubule lattice and the microtubule end.
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Authors find that 3D ECM engagement uncouples MCAK-mediated regulation of MT growth persistence from myosin-II-mediated regulation of growth persistence specifically within EC branched protrusions.
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REVIEW: Conformation changes in MCAK related to its depolymerization activity and function are described. A model of its regulation by multiple mitotic kinases is proposed and its potential involvement in oncogenesis and drug resistance its highlighted.
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GTSE1 inhibition of MCAK activity regulates the balance of MT stability that determines the fidelity of chromosome alignment, segregation, and chromosomal stability.
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MCAC role in microtubule assembly
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Our results reveal an underlying mechanism by which NuSAP controls kinetochore microtubule dynamics spatially and temporally by modulating the depolymerisation function of MCAK in an Aurora B kinase-dependent manner.
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MCAK is involved in directional migration and invasion of tumor cells.
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the Aurora B-PLK1 signaling at the kinetochore orchestrates MCAK activity, which is essential for timely correction of aberrant kinetochore attachment to ensure accurate chromosome segregation during mitosis.
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MCAK activity is modulated by Plk1 phosphorylation on S632/S633 in mitosis.
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These results demonstrate that the structural change of Kif2C-ATP upon binding to microtubule ends is sufficient for tubulin release, whereas ATP hydrolysis is not required
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Ras regulates KIF2C to control cell migration pathways in transformed human bronchial epithelial cells.
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A dynamic interaction of MCAK-TIP150 orchestrated by Aurora A-mediated phosphorylation governs entosis via regulating microtubule plus-end dynamics and cell rigidity.
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this study suggests a new mechanism by which Plk1 regulates MCAK: by regulating its degradation and hence controlling its turnover in mitosis.
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up-regulation of KIF2C and KIF2A by ERK1/2 caused aberrant lysosomal positioning and mTORC1 activity in a mutant K-Ras-dependent cancer and cancer model.
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A Rac1-Aurora A-MCAK signaling pathway mediates endothelial cell polarization and directional migration by promoting regional differences in microtubule dynamics.
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result suggested E403K mutation in mitotic centromere-associated kinesin protein as highly damaging and showed strong concordance to the previously observed colorectal cancer mutations aggregation tendency and energy value changes
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A CENP-E mediated wall-tethering event and a MCAK-mediated wall-removing event show that human chromosome-microtubule attachment is achieved through a set of deterministic sequential events rather than stochastic direct capture of microtubule ends.
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expression has no effect on the level of the TRAIL receptors DR4 and DR5. These findings might have clinical implications since the combination of TRAIL therapy with administration of Pgp modulators might sensitize TRAIL resistant tumors.
