NDLI: HSF1 regulates expression of G-CSF through the binding element for NF-IL6/CCAAT enhancer binding protein beta

Content Provider	SpringerLink
Author	Zhang, Lingli Yang, Mingshi Wang, Qiupeng Liu, Meidong Liang, Qiujuan Zhang, Huali Xiao, Xianzhong
Copyright Year	2011
Abstract	Heat shock factor 1 (HSF1) is the major heat shock transcription factor and plays an essential role in mediating the cellular response to physiological and environmental stress. We found that LPS-induced expression of the granulocyte-colony stimulating factor (G-CSF) gene was upregulated in HSF1 knock-out (HSF1$^{−/−}$) mice using a gene array. In order to determine whether and how HSF1 regulates the induced expression of G-CSF, mRNA, and protein levels of G-CSF were detected by Northern blotting and ELISA, the promoter of G-CSF was analyzed with an online transcription element search system and the transcriptional activity of the G-CSF promoter was analyzed by EMSA and a reporter gene assay. The results showed that transcription and protein secretion of G-CSF induced by LPS are both inhibited by HSF1. Three high affinity binding sites for NF-IL6/CCAAT enhancer binding protein beta, but no heat shock element, were identified in the core promoter of G-CSF. The DNA-binding capability of NF-IL6 to the G-CSF promoter was reinforced by LPS but not influenced by heat shock or HSF1. However, HSF1 was observed to bind to the binding sites of NF-IL6 in the G-CSF promoter. The transcriptional activity of the G-CSF promoter was enhanced by LPS or NF-IL6 and inhibited by HSF1 in a dose dependent manner. We conclude that HSF1 regulates expression of G-CSF through binding to the NF-IL6-binding element.
Starting Page	11
Ending Page	17
Page Count	7
File Format	PDF
ISSN	03008177
Journal	Molecular and Cellular Biochemistry
Volume Number	352
Issue Number	1-2
e-ISSN	15734919
Language	English
Publisher	Springer US
Publisher Date	2011-04-01
Publisher Place	Boston
Access Restriction	Subscribed
Subject Keyword	HSF1 G-CSF NF-IL6 CCAAT enhancer binding protein beta LPS Oncology Cardiology Medical Biochemistry Biochemistry
Content Type	Text
Resource Type	Article
Subject	Molecular Biology Clinical Biochemistry Cell Biology Medicine

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