KLF4 is a novel regulator of the constitutively expressed HSP90

被引:5
|
作者
Liu, Ying [1 ]
Liu, Meidong [1 ]
Liu, Junwen [1 ]
Zhang, Huali [1 ]
Tu, Zizhi [1 ]
Xiao, Xianzhong [1 ]
机构
[1] Cent S Univ, Dept Pathophysiol, Lab Shock, Xiangya Sch Med, Changsha 410008, Hunan, Peoples R China
来源
CELL STRESS & CHAPERONES | 2010年 / 15卷 / 02期
基金
中国国家自然科学基金;
关键词
KLF4; HSP90; HSP84; HSP86; Gene regulation; KRUPPEL-LIKE FACTOR-4; MYOBLAST DIFFERENTIATION; SIGNAL-TRANSDUCTION; DNA-DAMAGE; PROMOTER; KRUPPEL-LIKE-FACTOR-4; TRANSCRIPTION; MACROPHAGES; CELLS; SP1;
D O I
10.1007/s12192-009-0135-8
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Kruppel-like factor 4 (KLF4) is a zinc finger-containing transcription factor with diverse regulatory functions in cell growth, proliferation, and differentiation. But little is known about the regulation of KLF4 on the expression of HSP90 (HSP84 and HSP86). In the current study, overexpression of KLF4 was firstly identified to promote the basal expression of HSP90 (HSP84 and HSP86) but not the inducible expression in the C2C12 cells and RAW264.7 cells. Conversely, KLF4 inhibition by antisense oligonucleotides markedly decreased the constitutive expression of HSP90 (HSP84 and HSP86). Here, we also presented data that overexpression of KLF4 resulted in enhanced promoter activities of HSP84. Consistently, KLF4 bind to the KLF4 binding sites in the promoter regions of HSP84 directly. Together, these findings support a role for KLF4 as a novel regulator of the constitutive expression of HSP90.
引用
收藏
页码:211 / 217
页数:7
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