PBK/TOPK promotes tumour cell proliferation through p38 MAPK activity and regulation of the DNA damage response (Q40198127)

18 September 2017

PBK/TOPK promotes tumour cell proliferation through p38 MAPK activity and regulation of the DNA damage response (English)

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18 September 2017

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Ayllón V

1

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18 September 2017

O'connor R

series ordinal

2

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18 September 2017

language of work or name

English

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publication date

11 December 2006

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18 September 2017

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18 September 2017

26

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18 September 2017

3451-3461

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18 September 2017

24

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https://scigraph.springernature.com/pub.10.1038/sj.onc.1210142

18 September 2017

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Disruption of murine Mus81 increases genomic instability and DNA damage sensitivity but does not promote tumorigenesis

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PBK/TOPK, a proliferating neural progenitor-specific mitogen-activated protein kinase kinase

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Characterization of PDZ-binding kinase, a mitotic kinase

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Insulin-like growth factor-I (IGF-I) receptor activation rescues UV-damaged cells through a p38 signaling pathway. Potential role of the IGF-I receptor in DNA repair

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RACK1-mediated integration of adhesion and insulin-like growth factor I (IGF-I) signaling and cell migration are defective in cells expressing an IGF-I receptor mutated at tyrosines 1250 and 1251.

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ATM and DNA-PK function redundantly to phosphorylate H2AX after exposure to ionizing radiation

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Activated IGF-1R inhibits hyperglycemia-induced DNA damage and promotes DNA repair by homologous recombination

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21 January 2018

Identifiers

DOI

10.1038/SJ.ONC.1210142

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Dimensions Publication ID

18 September 2017

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