J Biol Chem. 2000 Dec 1;275(48):37469-73.

p53 and c-Jun functionally synergize in the regulation of the DNA repair gene hMSH2 in response to UV.

Scherer SJ, Maier SM, Seifert M, Hanselmann RG, Zang KD, Muller-Hermelink HK, Angel P, Welter C, Schartl M.

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Department of Human Genetics, University of Saarland, Geb. 68, D-66421 Homburg/Saar, Germany.

Abstract

The tumor suppresser protein p53 is critical for guarding the genome from incorporation of damaged DNA (Lane, D. P. (1992) Nature 358, 15-16). A relevant stress that activates p53 function is UV light (Noda, A., Toma-Aiba, Y., and Fujiwara, Y. (2000) Oncogene 19, 21-31). Another well known component of the mammalian UV response is the transcription factor c-Jun (Angel, P., and Karin, M. (1991) Biochim. Biophys. Acta 1072, 129-157). We show here that upon UV irradiation p53 activates transcription of the human mismatch repair gene MSH2. Interestingly, this up-regulation critically depends on functional interaction with c-Jun. Hence, the synergistic interaction of a proto-oncogene with a tumor suppresser gene is required for the regulation of the mammalian stress response through activation of expression of MSH2.

PMID:: 10984493; [PubMed - indexed for MEDLINE]

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p53 and c-Jun functionally synergize in the regulation of the DNA repair gene hMSH2 in response to UV.
J Biol Chem. 2000 Dec 1 ;275(48):37469-73.

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p53 and c-Jun functionally synergize in the regulation of the DNA repair gene hMSH2 in response to UV.

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