p53 deficiency enhances mitotic arrest and slippage induced by pharmacological inhibition of Aurora kinases (Q39108757)

9 September 2017

p53 deficiency enhances mitotic arrest and slippage induced by pharmacological inhibition of Aurora kinases (English)

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9 September 2017

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M Marxer

1

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9 September 2017

H T Ma

series ordinal

2

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9 September 2017

W Y Man

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3

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9 September 2017

R Y C Poon

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4

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9 September 2017

language of work or name

English

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publication date

19 August 2013

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33

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27

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9 September 2017

3550-3560

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https://scigraph.springernature.com/pub.10.1038/onc.2013.325

9 September 2017

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Discovery and exploitation of inhibitor-resistant aurora and polo kinase mutants for the analysis of mitotic networks

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Autophosphorylation of a newly identified site of Aurora-B is indispensable for cytokinesis

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Phosphorylation by aurora kinase A induces Mdm2-mediated destabilization and inhibition of p53.

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Characterization of Alisertib (MLN8237), an investigational small-molecule inhibitor of aurora A kinase using novel in vivo pharmacodynamic assays

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Aurora B couples chromosome alignment with anaphase by targeting BubR1, Mad2, and Cenp-E to kinetochores

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MK-5108, a highly selective Aurora-A kinase inhibitor, shows antitumor activity alone and in combination with docetaxel

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VX-680, a potent and selective small-molecule inhibitor of the Aurora kinases, suppresses tumor growth in vivo

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Validating Aurora B as an anti-cancer drug target.

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Aurora A and Aurora B jointly coordinate chromosome segregation and anaphase microtubule dynamics.

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Tetraploid state induces p53-dependent arrest of nontransformed mammalian cells in G1.

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Cytokinesis failure generating tetraploids promotes tumorigenesis in p53-null cells

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Cell cycle progression after cleavage failure: mammalian somatic cells do not possess a "tetraploidy checkpoint".

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Mammalian cells lack checkpoints for tetraploidy, aberrant centrosome number, and cytokinesis failure

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The consequences of tetraploidy and aneuploidy

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Aurora kinase A inhibition leads to p73-dependent apoptosis in p53-deficient cancer cells

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Gadd45a interacts with aurora-A and inhibits its kinase activity

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The Aurora kinase inhibitor VX-680 induces endoreduplication and apoptosis preferentially in cells with compromised p53-dependent postmitotic checkpoint function

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CDK1 inhibitors antagonize the immediate apoptosis triggered by spindle disruption but promote apoptosis following the subsequent rereplication and abnormal mitosis

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Determinants of mitotic catastrophe on abrogation of the G2 DNA damage checkpoint by UCN-01.

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inferred from DOI database lookup

7 January 2021

based on heuristic

Identifiers

DOI

10.1038/ONC.2013.325

1 reference

9 September 2017

1 reference