p300/CBP-dependent and -independent transcriptional interference between NF-κB RelA and p53

Akiko Ikeda, Xiangao Sun, Yan Li, Yong Kang Zhang, Richard Eckner, Takahiro S. Doi, Toshitada Takahashi, Yuichi Obata, Katsuji Yoshioka, Ken-ichi Yamamoto

Research output: Contribution to journalArticle

76 Citations (Scopus)

Abstract

p53 and NF-κB RelA are activated by various genotoxic agents and mutually suppress each other's ability to activate transcription, most likely through competition for transcriptional coactivators such as CBP or p300. However, we found that the inhibition by RelA of p53 transcriptional activity is not completely restored by CBP/p300 overexpression and that a p53 mutant can not suppress RelA activity despite of its ability to bind CBP/p300. In the present study, we further present evidence that these two transcriptional factors directly interact both in vivo and in vitro. These results therefore indicate that the cross transcriptional interference between p53 and RelA is partly caused by the direct interaction between these two transcription factors which is mediated by their dimerization/tetramerization domains and results in inhibition of each other's transcriptional activity. Finally, cells derived from RelA knockout mice showed enhanced p53 transcriptional activity, suggesting that this cross transcriptional interference is physiologically important in cellular response to genotoxic stress. (C) 2000 Academic Press.

Original languageEnglish
Pages (from-to)375-379
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume272
Issue number2
DOIs
Publication statusPublished - Jun 7 2000
Externally publishedYes

Fingerprint

Dimerization
Transcription
Knockout Mice
DNA Damage
Transcription Factors
In Vitro Techniques

Keywords

  • Genotoxic stress
  • Interaction
  • NF-κB
  • p53
  • Transcriptional interference

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

p300/CBP-dependent and -independent transcriptional interference between NF-κB RelA and p53. / Ikeda, Akiko; Sun, Xiangao; Li, Yan; Zhang, Yong Kang; Eckner, Richard; Doi, Takahiro S.; Takahashi, Toshitada; Obata, Yuichi; Yoshioka, Katsuji; Yamamoto, Ken-ichi.

In: Biochemical and Biophysical Research Communications, Vol. 272, No. 2, 07.06.2000, p. 375-379.

Research output: Contribution to journalArticle

Ikeda, A, Sun, X, Li, Y, Zhang, YK, Eckner, R, Doi, TS, Takahashi, T, Obata, Y, Yoshioka, K & Yamamoto, K 2000, 'p300/CBP-dependent and -independent transcriptional interference between NF-κB RelA and p53', Biochemical and Biophysical Research Communications, vol. 272, no. 2, pp. 375-379. https://doi.org/10.1006/bbrc.2000.2786
Ikeda, Akiko ; Sun, Xiangao ; Li, Yan ; Zhang, Yong Kang ; Eckner, Richard ; Doi, Takahiro S. ; Takahashi, Toshitada ; Obata, Yuichi ; Yoshioka, Katsuji ; Yamamoto, Ken-ichi. / p300/CBP-dependent and -independent transcriptional interference between NF-κB RelA and p53. In: Biochemical and Biophysical Research Communications. 2000 ; Vol. 272, No. 2. pp. 375-379.
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AU - Doi, Takahiro S.

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AB - p53 and NF-κB RelA are activated by various genotoxic agents and mutually suppress each other's ability to activate transcription, most likely through competition for transcriptional coactivators such as CBP or p300. However, we found that the inhibition by RelA of p53 transcriptional activity is not completely restored by CBP/p300 overexpression and that a p53 mutant can not suppress RelA activity despite of its ability to bind CBP/p300. In the present study, we further present evidence that these two transcriptional factors directly interact both in vivo and in vitro. These results therefore indicate that the cross transcriptional interference between p53 and RelA is partly caused by the direct interaction between these two transcription factors which is mediated by their dimerization/tetramerization domains and results in inhibition of each other's transcriptional activity. Finally, cells derived from RelA knockout mice showed enhanced p53 transcriptional activity, suggesting that this cross transcriptional interference is physiologically important in cellular response to genotoxic stress. (C) 2000 Academic Press.

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