Hypoxic inhibition of JMJD3 reduces H3K27me3 demethylation and induction of the STAT6 target gene CCL18
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- 作者：Nathalie Dehne ; dehne@biochem.uni-frankfurt.de" class="auth_mail" title="E-mail the corresponding author ; Bernhard Brü ; ne
- 关键词：C/EBPβ ; CCAAT/enhancer binding protein (C/EBP) ; beta ; c-myc ; MYC ; = ; v-myc avian myelocytomatosis viral oncogene homolog ; CBP ; CREBBP ; = ; CREB binding protein ; CCL18 ; chemokine (CC motif) ligand 18 (pulmonary and activation-regulated) ; CHX ; cycloheximid ; DMOG ; dimethyloxalylglycine ; F13A1 ; coagulation factor XIII A chain ; H3K4me1 ; histone 3 lysine 4 monomethylation ; H3K27ac ; histone 3 lysine 27 acetylation ; H3K27me3 ; histone 3 lysine 27 trimethylation ; HIF ; hypoxia-inducible fact
- 刊名：Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms
- 出版年：2016
- 出版时间：December 2016
- 年：2016
- 卷：1859
- 期：12
- 页码：1490-1501
- 全文大小：1718 K
文摘
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Hypoxia reduces the induction of CCL18 but not of SPINT2 without interfering with STAT6 activation.
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Removal of the repressive histone mark H3K27me3 is impaired at the CCL18 but not SPINT2 gene locus.
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JMJD3 is required for CCL18, but dispensable for SPINT2 induction.
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Hypoxia or DMOG reduces JMJD3 activity but not expression or cellular distribution.
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Recruitment of JMJD3 to the CCL18 gene is not facilitated by IRF4, KLF4, or PPARγ.