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These findings shed new light on the role of Kif18A in chromosome segregation and demonstrate that the spindle assembly checkpoint can be activated at kinetochores that are occupied by fully functional k-Mts that lack tension.
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KIF18A expression is a predictive biomarker of drug resistance to endocrine therapy in breast cancer.
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High KIF18A expression is associated with invasion and metastasis of hepatocellular carcinoma.
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Low post translational modifications of KIF18A protein is associated with neoplasms.
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KIF18a role in microtubule assembly
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Cdk1-mediated inhibitory phosphorylation of Kif18A promotes chromosome oscillations in early metaphase. PP1 induces metaphase plate thinning by directly dephosphorylating Kif18A.
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Confocal microscopy shows that cells expressing SUMO-resistant Kif18A display a compromised dissociation of BubR1 from kinetochores after anaphase onset.
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data support a model in which microtubule-attenuating kinesins are molecularly "tuned" to control the dynamics of specific subsets of spindle microtubules
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a biomarker for hepatocellular carcinoma diagnosis and an independent predictor of overall survival
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that the human mitotic kinesin-8, KIF18A, directly interacts with PP1gamma through a conserved RVxF motif
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the motion of yeast (Kip3) and human (Kif18A) kinesin-8s
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Mechanisms controlling the temporal degradation of Nek2A and Kif18A by the APC/C-Cdc20 complex.
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Kif18A (kinesin-8) attenuates centromere movement by directly promoting microtubule pausing in a concentration- dependent manner.
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there is a mutual regulation of kinetochore MT plus-end dynamics and Kif18A accumulation, which may contribute to the highly regulated and ordered changes in kinetochore spindle microtubule dynamics during chromosome congression and oscillation
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Kif18A controls spindle length independently of its role in chromosome positioning. This is mediated by an ATP-independent spindle microtubule (MT) binding site at C-terminal end of the Kif18A tail that has a strong affinity for MTs in vitro and in cells.
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The heightened processivity of Kif18A, conferred by its tail domain, thus promotes concentration of Kif18A at K-MT plus ends, where it suppresses their dynamics to control chromosome movements.
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Kif18A overexpression is associated with colorectal cancer progression.
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Kinesin (KIF18A) can be potentially used as a blood biomarker to identify asbestosis patients at risk of developing lung cancer.
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High Kif18A is associated with breast carcinogenesis.
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The kinesin-8 Kif18A dampens microtubule plus-end dynamics.