Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

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Transcription profiling of wild type, Trp53-null and Trp53-515C/515C (encoding p53R172P) mouse embryo fibroblasts treated with gamma-radiation


ABSTRACT: Trp53-null, Trp53-515C/515C (encoding p53R172P), or wild-type mouse embryo fibroblasts were treated with 6 Gy gamma-radiation and harvested 6 hours later to compare expression profiles of genes regulated by wild-type p53 and p53R172P. Trp53-null cells were included as a negative control.

ORGANISM(S): Mus musculus

SUBMITTER: Juan Barboza 

PROVIDER: E-MEXP-917 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

p21 delays tumor onset by preservation of chromosomal stability.

Barboza Juan A JA   Liu Geng G   Ju Zhenlin Z   El-Naggar Adel K AK   Lozano Guillermina G  

Proceedings of the National Academy of Sciences of the United States of America 20061214 52


The p53 protein suppresses tumorigenesis by initiating cellular functions such as cell cycle arrest and apoptosis in response to DNA damage. A p53 mutant, p53R172P, which is deficient for apoptosis but retains a partial cell cycle arrest function, delays tumor onset in mice. Remarkably, lymphomas arising in Trp53(515C/515C) mice (encoding p53R172P) retain stable genomes. Given the dominant role of p21 in p53 cell cycle control, we crossed Trp53(515C/515C) mice onto a p21-null background to deter  ...[more]

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