17 January, 2012
Volume 21, Issue 1
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Volume 21, Issue 1
On the cover: Id1high cells were sorted from PDGF-driven gliomas and plated at clonal density under nonadherent conditions to generate tumorspheres. Shown here is an individual tumorsphere that was differentiated and stained with the astrocyte marker GFAP. See Barrett et al., pp. 11–24, for more details.
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Volume 21 Issue 1: January 17, 2012
Featured Article
The featured article is freely available to all readers
Madhavsai Gajjar, Marco M. Candeias, Laurence Malbert-Colas, Anne Mazars, Jun Fujita, Vanesa Olivares-Illana, Robin Fåhraeus
The ATM kinase and p53 are key tumor suppressor factors that control the genotoxic stress response pathway. The ATM substrate Mdm2 controls p53 activity by either targeting p53 for degradation or promoting its synthesis by binding the p53 mRNA. The physiological role and regulation of Mdm2's dual function toward p53 is not known. Here we show that ATM-dependent phosphorylation of Mdm2 at Ser395 is required for the p53 mRNA-Mdm2 interaction. This event also promotes SUMO-conjugation of Mdm2 and its nucleoli accumulation. Interfering with the p53 mRNA-Mdm2 interaction prevents p53 stabilization and activation following DNA damage. These results demonstrate how ATM activity switches Mdm2 from a negative to a positive regulator of p53 via the p53 mRNA.
On the Cover
On the cover: Id1high cells were sorted from PDGF-driven gliomas and plated at clonal density under nonadherent conditions to generate tumorspheres. Shown here is an individual tumorsphere that was differentiated and stained with the astrocyte marker GFAP. See Barrett et al., pp. (pp. 11-24), for more details.
Next issue: February 13, 2012
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