Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases

被引:4071
作者
Johnson, GL [1 ]
Lapadat, R [1 ]
机构
[1] Univ Colorado, Hlth Sci Ctr, Dept Pharmacol, Denver, CO 80262 USA
关键词
Cells; -; Diseases; Physiology;
D O I
10.1126/science.1072682
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 [理学]; 0710 [生物学]; 09 [农学];
摘要
Multicellular organisms have three well-characterized subfamilies of mitogen-activated protein kinases (MAPKs) that control a vast array of physiological processes. These enzymes are regulated by a characteristic phosphorelay system in which a series of three protein kinases phosphorylate and activate one another. The extracellular signal-regulated kinases (ERKs) function in the control of cell division, and inhibitors of these enzymes are being explored as anticancer agents. The c-Jun amino-terminal kinases (JNKs) are critical regulators of transcription, and JNK inhibitors may be effective in control of rheumatoid arthritis. The p38 MAPKs are activated by inflammatory cytokines and environmental stresses and may contribute to diseases like asthma and autoimmunity.
引用
收藏
页码:1911 / 1912
页数:2
相关论文
共 11 条
[1]
Abe MK, 1999, MOL CELL BIOL, V19, P1301
[2]
Pharmacological inhibitors of MAPK pathways [J].
English, JM ;
Cobb, MH .
TRENDS IN PHARMACOLOGICAL SCIENCES, 2002, 23 (01) :40-45
[3]
MAPKK-independent activation of p38α mediated by TAB1-dependent autophosphorylation of p38α [J].
Ge, BX ;
Gram, H ;
Di Padova, F ;
Huang, B ;
New, L ;
Ulevitch, RJ ;
Luo, Y ;
Han, JH .
SCIENCE, 2002, 295 (5558) :1291-1294
[4]
C-Jun N-terminal kinase is required for metalloproteinase expression, and joint destruction in inflammatory arthritis [J].
Han, ZN ;
Boyle, DL ;
Chang, LF ;
Bennett, B ;
Karin, M ;
Yang, L ;
Manning, AM ;
Firestein, GS .
JOURNAL OF CLINICAL INVESTIGATION, 2001, 108 (01) :73-81
[5]
JOHNSON GL, 2002, SCI STKE
[6]
THE STRESS-ACTIVATED PROTEIN-KINASE SUBFAMILY OF C-JUN KINASES [J].
KYRIAKIS, JM ;
BANERJEE, P ;
NIKOLAKAKI, E ;
DAI, TA ;
RUBIE, EA ;
AHMAD, MF ;
AVRUCH, J ;
WOODGETT, JR .
NATURE, 1994, 369 (6476) :156-160
[7]
A PROTEIN-KINASE INVOLVED IN THE REGULATION OF INFLAMMATORY CYTOKINE BIOSYNTHESIS [J].
LEE, JC ;
LAYDON, JT ;
MCDONNELL, PC ;
GALLAGHER, TF ;
KUMAR, S ;
GREEN, D ;
MCNULTY, D ;
BLUMENTHAL, MJ ;
HEYS, JR ;
LANDVATTER, SW ;
STRICKLER, JE ;
MCLAUGHLIN, MM ;
SIEMENS, IR ;
FISHER, SM ;
LIVI, GP ;
WHITE, JR ;
ADAMS, JL ;
YOUNG, PR .
NATURE, 1994, 372 (6508) :739-746
[8]
INSULIN-STIMULATED MICROTUBULE-ASSOCIATED PROTEIN-KINASE IS PHOSPHORYLATED ON TYROSINE AND THREONINE INVIVO [J].
RAY, LB ;
STURGILL, TW .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1988, 85 (11) :3753-3757
[9]
Requirement of JNK for stress-induced activation of the cytochrome c-mediated death pathway [J].
Tournier, C ;
Hess, P ;
Yang, DD ;
Xu, J ;
Turner, TK ;
Nimnual, A ;
Bar-Sagi, D ;
Jones, SN ;
Flavell, RA ;
Davis, RJ .
SCIENCE, 2000, 288 (5467) :870-874
[10]
Mitogen-activated protein kinase: Conservation of a three-kinase module from yeast to human [J].
Widmann, C ;
Gibson, S ;
Jarpe, MB ;
Johnson, GL .
PHYSIOLOGICAL REVIEWS, 1999, 79 (01) :143-180