UP-REGULATION OF ERK (MAP KINASE) AND MEM (MAP KINASE KINASE) TRANSCRIPTION AFTER RAT FACIAL-NERVE TRANSECTION

被引:29
作者
KITAHARA, T
KIRYU, S
OHNO, K
MORITA, N
KUBO, T
KIYAMA, H
机构
[1] OSAKA UNIV,SCH MED,BIOMED RES CTR,DEPT NEUROANAT,SUITA,OSAKA 565,JAPAN
[2] OSAKA UNIV,SCH MED,DEPT OTOLARYNGOL,SUITA,OSAKA 565,JAPAN
关键词
RAS PATHWAY; GROWTH FACTOR RECEPTOR; REGENERATION; AXOTOMY; IN SITU HYBRIDIZATION; IMMUNOHISTOCHEMISTRY;
D O I
10.1016/0168-0102(94)90097-3
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Up-regulation of ERK (extracellular signal-regulated kinase or MAP kinase) and MEK (ERK kinase or MAPK kinase) expression after rat facial nerve injury was demonstrated by in situ hybridization histochemistry and immunohistochemistry. These two enzymes play roles in one of the major intracellular signal cascade pathways involving receptor tyrosine kinase common to growth factor receptors, and transcription factors. Significant increases in ERK1 mRNA levels were observed from day 3 after facial nerve transection, with the highest level of expression from 1 to 2 weeks after the operation. This high level of mRNA expression then decreased gradually to the normal level. ERK1-like immunoreactivity showed a similar time course to that of its mRNA expression; however, the decay profile was more prolonged. The up-regulation of MEK, the ERK kinase/MAPK kinase, was also detected by immunohistochemistry. The protein expression profiles were almost equivalent, but the MEK expression was slightly advanced, suggesting that the observed up-regulation of MEK was not due to that of ERK. The receptor tyrosine kinase signal transduction pathway via MEK-ERK located downstream of growth factor receptors seems vital as a regulator of the synthesis of molecules that play important roles in the recovery process following injury or/and regeneration.
引用
收藏
页码:275 / 280
页数:6
相关论文
共 31 条
[1]  
AHN NG, 1990, J BIOL CHEM, V265, P11487
[2]  
AHN NG, 1990, J BIOL CHEM, V265, P11495
[3]  
BARDE YA, 1989, NEURON, V2, P1524
[4]   CLOSING IN ON SH2 SPECIFICITY [J].
BIRGE, RB ;
HANAFUSA, H .
SCIENCE, 1993, 262 (5139) :1522-1523
[5]   AN INSULIN-STIMULATED PROTEIN-KINASE SIMILAR TO YEAST KINASES INVOLVED IN CELL-CYCLE CONTROL [J].
BOULTON, TG ;
YANCOPOULOS, GD ;
GREGORY, JS ;
SLAUGHTER, C ;
MOOMAW, C ;
HSU, J ;
COBB, MH .
SCIENCE, 1990, 249 (4964) :64-67
[6]   ERKS - A FAMILY OF PROTEIN-SERINE THREONINE KINASES THAT ARE ACTIVATED AND TYROSINE PHOSPHORYLATED IN RESPONSE TO INSULIN AND NGF [J].
BOULTON, TG ;
NYE, SH ;
ROBBINS, DJ ;
IP, NY ;
RADZIEJEWSKA, E ;
MORGENBESSER, SD ;
DEPINHO, RA ;
PANAYOTATOS, N ;
COBB, MH ;
YANCOPOULOS, GD .
CELL, 1991, 65 (04) :663-675
[7]   GROWTH-FACTOR SIGNALING - WHERE IS THE SPECIFICITY [J].
CHAO, MV .
CELL, 1992, 68 (06) :995-997
[8]   MOUSE ERK-1 GENE-PRODUCT IS A SERINE THREONINE PROTEIN-KINASE THAT HAS THE POTENTIAL TO PHOSPHORYLATE TYROSINE [J].
CREWS, CM ;
ALESSANDRINI, AA ;
ERIKSON, RL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (19) :8845-8849
[9]   THE PRIMARY STRUCTURE OF MEK, A PROTEIN-KINASE THAT PHOSPHORYLATES THE ERK GENE-PRODUCT [J].
CREWS, CM ;
ALESSANDRINI, A ;
ERIKSON, RL .
SCIENCE, 1992, 258 (5081) :478-480
[10]  
DAVIS RJ, 1993, J BIOL CHEM, V268, P14553