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Increased radioresistance and accelerated B cell lymphomas in mice with Mdmx mutations that prevent modifications by DNA-damage-activated kinases.

Abstract：

:Mdmx is a critical negative regulator of the p53 pathway that is stoichiometrically limiting in some tissues. Posttranslational modification and degradation of Mdmx after DNA damage have been proposed to be essential for p53 activation. We tested this model in vivo, where critical stoichiometric relationships are preserved. We generated an Mdmx mutant mouse in which three conserved serines (S341, S367, S402) targeted by DNA-damage-activated kinases were replaced by alanines to investigate whether modifications of these residues are important for Mdmx degradation and p53 activation. The mutant mice were remarkably resistant to radiation, and very susceptible to Myc-induced lymphomagenesis. These data demonstrate that Mdmx downregulation is crucial for effective p53-mediated radiation responses and tumor suppression in vivo.

journal_name

Cancer Cell

journal_title

Cancer cell

authors

Wang YV,Leblanc M,Wade M,Jochemsen AG,Wahl GM

doi

10.1016/j.ccr.2009.05.008

subject

Has Abstract

pub_date

2009-07-07 00:00:00

pages

33-43

issue

1

eissn

1535-6108

issn

1878-3686

pii

S1535-6108(09)00174-3

journal_volume

16

pub_type

杂志文章

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