title: Modification of glucocorticoid sensitivity by MAP kinase signaling pathways in glucocorticoid-induced T-cell apoptosis.
abstract: 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.
  
  
  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.
  
  
  CONCLUSIONS
  These findings might provide new tools for overcoming glucocorticoid-resistance.
authors.affiliation: Department of Medicine and Bioregulatory Science, Graduate School of Medical Science, Kyushu University, Fukuoka, Japan.
authors.forename: Tomoko
authors.initials: T
authors.lastname: Tanaka
authors.forename: Taijiro
authors.initials: T
authors.lastname: Okabe
authors.forename: Shigeki
authors.initials: S
authors.lastname: Gondo
authors.forename: Mitsue
authors.initials: M
authors.lastname: Fukuda
authors.forename: Masahiro
authors.initials: M
authors.lastname: Yamamoto
authors.forename: Tsukuru
authors.initials: T
authors.lastname: Umemura
authors.forename: Kenzaburo
authors.initials: K
authors.lastname: Tani
authors.forename: Masatoshi
authors.initials: M
authors.lastname: Nomura
authors.forename: Kiminobu
authors.initials: K
authors.lastname: Goto
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Yanase
authors.forename: Hajime
authors.initials: H
authors.lastname: Nawata
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D051017:Apoptosis Regulatory Proteins / Q000096:biosynthesis; D002070:Butadienes / Q000494:pharmacology; D045744:Cell Line, Tumor; D003907:Dexamethasone / Q000494:pharmacology; D004789:Enzyme Activation / Q000187:drug effects; D005938:Glucocorticoids / Q000494:pharmacology*; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors* / Q000378:metabolism; D009570:Nitriles / Q000494:pharmacology; D011725:Pyridines / Q000494:pharmacology; D012680:Sensitivity and Specificity; D015398:Signal Transduction / Q000187:drug effects*; D013601:T-Lymphocytes / Q000187:drug effects* / Q000378:metabolism
chemical_list: D051017:Apoptosis Regulatory Proteins; D002070:Butadienes; D005938:Glucocorticoids; D007093:Imidazoles; D009570:Nitriles; D011725:Pyridines; C113580:U 0126; D003907:Dexamethasone; D020928:Mitogen-Activated Protein Kinases; C093642:SB 203580