ΔFosB, but not FosB, induces delayed apoptosis independent of cell proliferation in the Rat1a embryo cell line

K. Tahara, D. Tsuchimoto, Y. Tominaga, S. Asoh, S. Ohta, M. Kitagawa, H. Horie, T. Kadoya, Yusaku Nakabeppu

研究成果: Contribution to journalArticle査読

24 被引用数 (Scopus)

抄録

The fates of Rat1a cells expressing FosB and ΔFosB as fusion proteins (ER-FosB, ER-ΔFosB) with the ligand binding domain of human estrogen receptor were examined. The binding of estrogen to the fusion proteins resulted in their nuclear translocation and triggered cell proliferation, and thereafter delayed cell death was observed only in cells expressing ER-ΔFosB. The proliferation of Rat1a cells, but not cell death triggered by ER-ΔFosB, was completely abolished by butyrolactone I, an inhibitor of cycline-dependent kinases, and was partly suppressed by antisense oligonucleotides against galectin-1, whose expression is induced after estrogen administration. The cell death was accompanied by the activation of caspase-3 and -9, the fragmentation of the nuclear genome and cytochrome c release from the mitochondria, and was suppressed by zDEVD-fmk and zLEHD-fmk but not zIETD-fmk. The cell death was not suppressed by exogenous His-PTD-Bcl-xL at all, suggesting involvement of a Bcl-xL-resistant pathway for cytochrome c release.

本文言語英語
ページ(範囲)496-507
ページ数12
ジャーナルCell Death and Differentiation
10
5
DOI
出版ステータス出版済み - 5 1 2003

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cell Biology

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