Crosstalk between glucocorticoids and mitogen-activated protein kinase signalling pathways

被引：98

作者：

Clark, AR ^{[1
]}

Lasa, M ^{[1
]}

机构：

[1] Univ London Imperial Coll Sci Technol & Med, Fac Med, Kennedy Inst Rheumatol Div, London W6 8LH, England

来源：

CURRENT OPINION IN PHARMACOLOGY | 2003年 / 3卷 / 04期

基金：

英国医学研究理事会;

关键词：

D O I：

10.1016/S1471-4892(03)00073-0

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Synthetic glucocorticoids are potent modulators of the immune system, and are clinically invaluable in the treatment of a wide variety of conditions. However, their use can be limited by harmful side effects, and their mechanisms of action remain poorly understood and controversial. It has recently been reported that glucocorticoids induce the expression of two genes that participate in cross-talk with the mitogen-activated protein kinase signalling pathways. It is possible that both therapeutic and harmful effects of glucocorticoids may be mediated by these genes.

引用

页码：404 / 411

页数：8

共 83 条

[71] Human DU145 prostate cancer cells overexpressing mitogen-activated protein kinase phosphatase-1 are resistant to Fas ligand-induced mitochondrial perturbations and cellular apoptosis
Srikanth, S
Franklin, CC
Duke, RC
Kraft, AS
[J]. MOLECULAR AND CELLULAR BIOCHEMISTRY, 1999, 199 (1-2) : 169 - 178
[72] Jun N-terminal kinase stress-activated protein kinase (JNK/SAPK) is required for lipopolysaccharide stimulation of tumor necrosis factor alpha (TNF-alpha) translation: Glucocorticoids inhibit TNF-alpha translation by blocking JNK/SAPK
Swantek, JL
Cobb, MH
Geppert, TD
[J]. MOLECULAR AND CELLULAR BIOLOGY, 1997, 17 (11) : 6274 - 6282
[73] Regulation of stress-activated protein kinase signaling pathways by protein phosphatases
Tamura, S
Hanada, M
Ohnishi, M
Katsura, K
Sasaki, M
Kobayashi, T
[J]. EUROPEAN JOURNAL OF BIOCHEMISTRY, 2002, 269 (04): : 1060 - 1066
[74] The nucleosomal response associated with immediate-early gene induction is mediated via alternative MAP kinase cascades: MSK1 as a potential histone H3/HMG-14 kinase
Thomson, S
Clayton, AL
Hazzalin, CA
Rose, S
Barratt, MJ
Mahadevan, LC
[J]. EMBO JOURNAL, 1999, 18 (17) : 4779 - 4793
[75] Gene expression profiles of proliferating vs. G1/G0 arrested human leukemia cells suggest a mechanism for glucocorticoid-induced apoptosis
Tonko, M
Ausserlechner, MJ
Bernhard, D
Helmberg, A
Kofler, R
[J]. FASEB JOURNAL, 2001, 15 (03) : 693 - 699
[76] The DNA binding-independent function of the glucocorticoid receptor mediates repression of AP-1-dependent genes in skin
Tuckermann, JP
Reichardt, HM
Arribas, R
Richter, KH
Schütz, G
Angel, P
[J]. JOURNAL OF CELL BIOLOGY, 1999, 147 (07) : 1365 - 1370
[77] Vanden Berghe W, 1999, MOL PHARMACOL, V56, P797
[78] Synthetic glucocorticoids that dissociate transactivation and AP-1 transrepression exhibit antiinflammatory activity in vivo
Vayssiere, BM
Dupont, S
Choquart, A
Petit, F
Garcia, T
Marchandeau, C
Gronemeyer, H
RescheRigon, M
[J]. MOLECULAR ENDOCRINOLOGY, 1997, 11 (09) : 1245 - 1255
[79] Transcriptional activation of the NF-κB p65 subunit by mitogen- and stress-activated protein kinase-1 (MSK1)
Vermeulen, L
De Wilde, G
Van Damme, P
Vanden Berghe, W
Haegeman, G
[J]. EMBO JOURNAL, 2003, 22 (06) : 1313 - 1324
[80] Glucocorticoid receptor interaction with 14-3-3 and Raf-1, a proposed mechanism for cross-talk of two signal transduction pathways
Widén, C
Zilliacus, J
Gustafsson, JÅ
Wikström, AC
[J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (50) : 39296 - 39301

← 1 2 3 4 5 6 7 8 9 →