Modification of glucocorticoid sensitivity by MAP kinase signaling pathways in glucocorticoid-induced T-cell apoptosis

Tomoko Tanaka, Taijiro Okabe, Shigeki Gondo, Mitsue Fukuda, Masahiro Yamamoto, Tsukuru Umemura, Kenzaburo Tani, Masatoshi Nomura, Kiminobu Goto, Toshihiko Yanase, Hajime Nawata

研究成果: Contribution to journalArticle査読

18 被引用数 (Scopus)

抄録

Objective: Glucocorticoid is widely used for the treatment of diseases such as hematological malignancies. Glucocorticoid sensitivity is different from person to person and the mechanism of the regulation of glucocorticoid sensitivity is not well known. Glucocorticoid resistance is a major clinical problem. Methods and Results: Here, using glucocorticoid-induced T-cell apoptosis, a model system for the analysis of the mechanism of glucocorticoid action, we clarified that mitogen-activated protein kinases (MAPKs) modify glucocorticoid sensitivity, namely that the activation of extracellular signal-regulated protein kinase (ERK) and p38 MAP kinase reduce and enhance glucocorticoid sensitivity, respectively. Conclusion: These findings might provide new tools for overcoming glucocorticoid-resistance.

本文言語英語
ページ(範囲)1542-1552
ページ数11
ジャーナルExperimental Hematology
34
11
DOI
出版ステータス出版済み - 11 2006

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Hematology
  • Genetics
  • Cell Biology
  • Cancer Research

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