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Kinesin family member 18A

Kif18A, MS-KIF18A, kinesin family member 18A
KIF18A is a member of the kinesin superfamily of microtubule-associated molecular motors (see MIM 148760) that use hydrolysis of ATP to produce force and movement along microtubules (Luboshits and Benayahu, 2005 [PubMed 15878648]).[supplied by OMIM, Aug 2008] (from NCBI)
Top mentioned proteins: V1a, KIF4, HAD, OUT, CAN
Papers on Kif18A
Combined expressional analysis, bioinformatics and targeted proteomics identify new potential therapeutic targets in glioblastoma stem cells.
Langmoen et al., Oslo, Norway. In Oncotarget, Oct 2015
Bioinformatic filtering identified 20 genes (PBK/TOPK, CENPA, KIF15, DEPDC1, CDC6, DLG7/DLGAP5/HURP, KIF18A, EZH2, HMMR/RHAMM/CD168, NOL4, MPP6, MDM1, RAPGEF4, RHBDD1, FNDC3B, FILIP1L, MCC, ATXN7L4/ATXN7L1, P2RY5/LPAR6 and FAM118A) that were consistently expressed in GSC cultures and consistently not expressed in NSC cultures.
Biased Brownian motion as a mechanism to facilitate nanometer-scale exploration of the microtubule plus end by a kinesin-8.
Ohi et al., Nashville, United States. In Proc Natl Acad Sci U S A, Aug 2015
Well-characterized members of this subfamily (Kip3, Kif18A) exhibit two important properties: (i) They are "ultraprocessive," a feature enabled by a second MT-binding site that tethers the motors to a MT track, and (ii) they dissociate infrequently from the plus end.
Kif18a is specifically required for mitotic progression during germ line development.
Reinholdt et al., Bar Harbor, United States. In Dev Biol, Jul 2015
Here we show that the underlying mutation is a mis-sense mutation, R308K, in the motor domain of the kinesin-8 family member, KIF18A, a protein that is expressed in a variety of proliferative tissues and is a key regulator of chromosome alignment during mitosis.
Synthesis and biological evaluation of optimized inhibitors of the mitotic kinesin Kif18A.
Mayer et al., Konstanz, Germany. In Acs Chem Biol, Mar 2015
In this study, we report the identification of optimized small molecule inhibitors of the mitotic kinesin Kif18A.
Sumoylation of Kif18A plays a role in regulating mitotic progression.
Dai et al., New York City, United States. In Bmc Cancer, 2014
BACKGROUND: Kif18A, the kinesin-8 motor protein, plays an essential role in regulating alignment of bi-oriented chromosomes at the midzone during mitosis.
High KIF18A expression correlates with unfavorable prognosis in primary hepatocellular carcinoma.
Wang et al., Guilin, China. In Oncotarget, 2014
This study aimed to investigate KIF18A expression in hepatocellular carcinoma (HCC) and to determine the possibility of KIF18A expression being a biomarker in HCC diagnosis or being an independent predictor of disease-free survival (DFS) and overall survival (OS) in HCC patients underwent surgical resection.
A unique kinesin-8 surface loop provides specificity for chromosome alignment.
Stumpff et al., Burlington, United States. In Mol Biol Cell, 2014
Kif18A (kinesin-8) localizes to the plus ends of the relatively slowly growing kinetochore fibers (K-fibers) and attenuates their dynamics, whereas Kif4A (kinesin-4) localizes to mitotic chromatin and suppresses the growth of highly dynamic, nonkinetochore microtubules.
The human mitotic kinesin KIF18A binds protein phosphatase 1 (PP1) through a highly conserved docking motif.
Moorhead et al., Calgary, Canada. In Biochem Biophys Res Commun, 2014
Here we show that the human mitotic kinesin-8, KIF18A, directly interacts with PP1γ through a conserved RVxF motif.
Metastatic potential is determined early in synovial sarcoma development and reflected by tumor molecular features.
Debiec-Rychter et al., Warsaw, Poland. In Int J Biochem Cell Biol, 2014
RESULTS: AURKA and KIF18A, which play important roles in various mitotic events, were the two most up-regulated genes in SynSa2 and SynSa3 groups compared to the SynSa1 group.
Kinesin family deregulation coordinated by bromodomain protein ANCCA and histone methyltransferase MLL for breast cancer cell growth, survival, and tamoxifen resistance.
Chen et al., Sacramento, United States. In Mol Cancer Res, 2014
Estrogen strongly induces expression of 19 kinesin genes such as Kif4A/4B, Kif5A/5B, Kif10, Kif11, Kif15, Kif18A/18B, Kif20A/20B, Kif21, Kif23, Kif24, Kif25, and KifC1, whereas suppresses the expression of seven others, including Kif1A, Kif1C, Kif7, and KifC3.
Co-regulation proteomics reveals substrates and mechanisms of APC/C-dependent degradation.
Steen et al., Boston, United States. In Embo J, 2014
Biochemical studies on the kinesins confirmed KIFC1, KIF18A, KIF2C, and KIF4A as APC/C substrates.
Transactivating mutation of the MYOD1 gene is a frequent event in adult spindle cell rhabdomyosarcoma.
Hogendoorn et al., Leiden, Netherlands. In J Pathol, 2014
MYOD1, KIF18A, NOTCH1, and EML5 were further tested for mutations using Sanger sequencing on DNA from FFPE samples from 16 additional, adult spindle cell RMS samples.
Pre-anaphase chromosome oscillations are regulated by the antagonistic activities of Cdk1 and PP1 on Kif18A.
Mayer et al., Konstanz, Germany. In Nat Commun, 2013
Kinesin-8 Kif18A has been identified as a suppressor of chromosome movements, but how its activity is temporally regulated to dampen chromosome oscillations before anaphase onset remained mysterious.
Targeted deletion of Kif18a protects from colitis-associated colorectal (CAC) tumors in mice through impairing Akt phosphorylation.
Wang et al., Shanghai, China. In Biochem Biophys Res Commun, 2013
Here, we demonstrate that the kinesin-8 Kif18a is overexpressed in murine CAC and is a crucial promoter during early CAC carcinogenesis.
Kif18A and chromokinesins confine centromere movements via microtubule growth suppression and spatial control of kinetochore tension.
Wordeman et al., Seattle, United States. In Dev Cell, 2012
Kif18A (kinesin-8) attenuates centromere movement by directly promoting microtubule pausing in a concentration- dependent manner.
Kif18A uses a microtubule binding site in the tail for plus-end localization and spindle length regulation.
Walczak et al., Bloomington, United States. In Curr Biol, 2011
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.
A tethering mechanism controls the processivity and kinetochore-microtubule plus-end enrichment of the kinesin-8 Kif18A.
Ohi et al., Seattle, United States. In Mol Cell, 2011
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.
Proteomic detection of cancer in asbestosis patients using SELDI-TOF discovered serum protein biomarkers.
Brandt-Rauf et al., Aurora, United States. In Biomarkers, 2011
Kinesin (KIF18A) can be potentially used as a blood biomarker to identify asbestosis patients at risk of developing lung cancer.
Microtubule stabilization triggers the plus-end accumulation of Kif18A/kinesin-8.
Ohsugi et al., Tokyo, Japan. In Cell Struct Funct, 2010
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
Kinesin-8 molecular motors: putting the brakes on chromosome oscillations.
Bloom et al., Minneapolis, United States. In Trends Cell Biol, 2008
Recent studies suggest that the human Kinesin-8 molecular motor Kif18A has a role in chromosome congression.
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