Evidence that mitotic exit is a better cancer therapeutic target than spindle assembly. - Wikidata - awgldk - TriplyDB

Evidence that mitotic exit is a better cancer therapeutic target than spindle assembly.

Evidence that mitotic exit is a better cancer therapeutic target than spindle assembly.

http://www.wikidata.org/entity/Q42128896

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SIK2 is a centrosome kinase required for bipolar mitotic spindle formation that provides a potential target for therapy in ovarian cancer Live-cell imaging RNAi screen identifies PP2A-B55alpha and importin-beta1 as key mitotic exit regulators in human cells Pharmacologic inhibition of the anaphase-promoting complex induces a spindle checkpoint-dependent mitotic arrest in the absence of spindle damage APC15 drives the turnover of MCC-CDC20 to make the spindle assembly checkpoint responsive to kinetochore attachment Insights into APC/C: from cellular function to diseases and therapeutics Antiproliferative Fate of the Tetraploid Formed after Mitotic Slippage and Its Promotion; A Novel Target for Cancer Therapy Based on Microtubule Poisons An Overview of Alternating Electric Fields Therapy (NovoTTF Therapy) for the Treatment of Malignant Glioma New Auroras on the Roles of the Chromosomal Passenger Complex in Cytokinesis: Implications for Cancer Therapies Targeting the Mitotic Catastrophe Signaling Pathway in Cancer K11-linked ubiquitin chains as novel regulators of cell division Mitotic Spindle Disruption by Alternating Electric Fields Leads to Improper Chromosome Segregation and Mitotic Catastrophe in Cancer Cells.Inhibitors of phosphatidylinositol 3'-kinases promote mitotic cell death in HeLa cells The 3' untranslated region of the cyclin B mRNA is not sufficient to enhance the synthesis of cyclin B during a mitotic block in human cells Parkin Regulates Mitosis and Genomic Stability through Cdc20/Cdh1.Tumor treating fields perturb the localization of septins and cause aberrant mitotic exit Uncoordinated loss of chromatid cohesion is a common outcome of extended metaphase arrest Targeting of Fzr/Cdh1 for timely activation of the APC/C at the centrosome during mitotic exit.Structural analysis of human Cdc20 supports multisite degron recognition by APC/C Selective Aurora Kinase Inhibitors Identified Using a Taxol-Induced Checkpoint Sensitivity Screen Cdk1 promotes kinetochore bi-orientation and regulates Cdc20 expression during recovery from spindle checkpoint arrest APC/C and retinoblastoma interaction: cross-talk of retinoblastoma protein with the ubiquitin proteasome pathway Stochastic competition between mechanistically independent slippage and death pathways determines cell fate during mitotic arrest HSP90 inhibition enhances antimitotic drug-induced mitotic arrest and cell death in preclinical models of non-small cell lung cancer Cell Division Cycle 6 Promotes Mitotic Slippage and Contributes to Drug Resistance in Paclitaxel-Treated Cancer Cells The APC/C recruits cyclin B1-Cdk1-Cks in prometaphase before D box recognition to control mitotic exit Different cell fates after mitotic slippage: From aneuploidy to polyploidy Rapid induction of apoptosis during Kinesin-5 inhibitor-induced mitotic arrest in HL60 cells.Prolonged mitotic arrest triggers partial activation of apoptosis, resulting in DNA damage and p53 induction The microtubule poison vinorelbine kills cells independently of mitotic arrest and targets cells lacking the APC tumour suppressor more effectively.Temporal competition between differentiation programs determines cell fate choice.Leukemia-associated RhoGEF (LARG) is a novel RhoGEF in cytokinesis and required for the proper completion of abscission.Differential determinants of cancer cell insensitivity to antimitotic drugs discriminated by a one-step cell imaging assay Kinetic framework of spindle assembly checkpoint signalling Synergistic blockade of mitotic exit by two chemical inhibitors of the APC/C.The NOXA-MCL1-BIM axis defines lifespan on extended mitotic arrest Defective sister chromatid cohesion is synthetically lethal with impaired APC/C function.Cdc20: a potential novel therapeutic target for cancer treatment Synergistic activity of the histone deacetylase inhibitor trichostatin A and the proteasome inhibitor PS-341 against taxane-resistant ovarian cancer cell lines APC(Cdc20) suppresses apoptosis through targeting Bim for ubiquitination and destruction.Plk1 phosphorylation of CAP-H2 triggers chromosome condensation by condensin II at the early phase of mitosis.

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Evidence that mitotic exit is a better cancer therapeutic target than spindle assembly.

http://www.wikidata.org/entity/Q42128896

description

2009 nî lūn-bûn

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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2009年论文

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2009年论文

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name

Evidence that mitotic exit is a better cancer therapeutic target than spindle assembly.

@en

Evidence that mitotic exit is a better cancer therapeutic target than spindle assembly.

@nl

type

label

Evidence that mitotic exit is a better cancer therapeutic target than spindle assembly.

@en

Evidence that mitotic exit is a better cancer therapeutic target than spindle assembly.

@nl

prefLabel

Evidence that mitotic exit is a better cancer therapeutic target than spindle assembly.

@en

Evidence that mitotic exit is a better cancer therapeutic target than spindle assembly.

@nl

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J.CCR.2009.08.020

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Evidence that mitotic exit is a better cancer therapeutic target than spindle assembly

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Hsiao-Chun Huang

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Timothy J Mitchison

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P2860

Anaphase initiation is regulated by antagonistic ubiquitination and deubiquitination activities

BH3 profiling identifies three distinct classes of apoptotic blocks to predict response to ABT-737 and conventional chemotherapeutic agents

Genetic Control of the Cell Division Cycle in Yeast: V. Genetic Analysis of cdc Mutants

Mitotic checkpoint slippage in humans occurs via cyclin B destruction in the presence of an active checkpoint.

Quantitative live imaging of cancer and normal cells treated with Kinesin-5 inhibitors indicates significant differences in phenotypic responses and cell fate

The APC/C maintains the spindle assembly checkpoint by targeting Cdc20 for destruction.

The small molecule Hesperadin reveals a role for Aurora B in correcting kinetochore-microtubule attachment and in maintaining the spindle assembly checkpoint

The spindle-assembly checkpoint in space and time

Small molecule inhibitor of mitotic spindle bipolarity identified in a phenotype-based screen

Microtubules as a target for anticancer drugs

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