Gene expression of CCAAT/enhancer-binding protein δ mediated by autoregulation is repressed by related gene family proteins

Atsuhiro Tanabe, Chizumi Kumahara, Shigehiro Osada, Tsutomu Nishihara, Masayoshi Imagawa

Research output: Contribution to journalArticle

4 Citations (Scopus)


CCAAT/enhancer-binding protein δ (C/EBPδ) transcription factor is rapidly induced at an early stage of acute phase response. We previously reported that this induction was mainly mediated by acute phase response factor/signal transducers and activators of transcription 3 (APRF/STAT3). Furthermore, the high expression level of C/EBPδ is maintained by autoregulation mechanisms through the C/EBPδ binding sites located downstream of C/EBPδ gene. Thereafter, the expression of C/EBPδ gene decreases rapidly to the basal level. However, these mechanisms are still unknown. According to both transfection and DNA binding analyses, liver-enriched inhibitory protein (LIP), the shorter form of C/EBPβ and C/EBP-homologous protein 10 (CHOP10), were found to inhibit C/EBPδ gene expression. DNA binding analysis has further indicated that both LIP and CHOP10 form heterodimers with C/EBPδ, and inhibit the binding of C/EBPδ homodimer to the C/EBPδ binding sites located downstream of C/EBPδ gene. Taken together, these findings indicated that the maintained expression of C/EBPδ gene by autoregulation was inhibited and decreased to the basal level as a result of the competition of other C/EBP family proteins. Thus, C/EBPδ gene expression is mediated by the gene regulation circuit through the downstream C/EBPδ binding sites.

Original languageEnglish
Pages (from-to)1424-1429
Number of pages6
JournalBiological and Pharmaceutical Bulletin
Issue number12
Publication statusPublished - 2000 Jan 1



  • Autoregulation
  • CCAAT/enhancer-binding protein
  • CHOP
  • Gene expression
  • Trans-acting factor
  • Transcription

ASJC Scopus subject areas

  • Pharmacology
  • Pharmaceutical Science

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