Activation of the MKK4‐JNK pathway during erythroid differentiation of K562 cells is inhibited by the heat shock factor 2‐β isoform

FEBS Letters

Coffey, Eleanor T.¹  Elo, Iina¹  Eriksson, John E.¹  Rosenström, Heidi¹  Hietakangas, Ville¹  Kyriakis, John M.²  Sistonen, Lea¹ 

[1] Turku Centre for Biotechnology, University of Turku, Åbo Akademi University, P.O. Box 123, FIN-20521 Turku, Finland;Diabetes Research Laboratory, Massachusetts General Hospital, MGH East 149 13th Street, Charlestown, MA 02129, USA

关键词: Heat shock factor 2;    JNK/SAPK;    Erythroid differentiation;    Hemin;    K562 cell;    Mitogen-activated protein kinase;   

DOI  :  10.1016/S0014-5793(01)02810-1

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

In this study we report the activation of c-Jun N-terminal kinase (JNK) in human K562 erythroleukemia cells undergoing hemin-mediated erythroid differentiation, which occurs concomitantly with activation of heat shock factor 2 (HSF2) and leads to a simultaneous in vivo phosphorylation of c-Jun. The activation of JNK occurs through activation of mitogen-activated protein kinase kinase (MKK) 4 and not by activation of MKK7 or inhibition of JNK-directed phosphatases. We have previously shown that overexpression of the HSF2-β isoform inhibits the activation of HSF2 upon hemin-induced erythroid differentiation. Here we demonstrate that HSF2-β overexpression blocks the hemin-induced activation of the MKK4-JNK pathway, suggesting an erythroid lineage-specific JNK activation likely to be regulated by HSF2.

【 授权许可】

Unknown