التفاصيل البيبلوغرافية
| العنوان: |
Gene networking and inflammatory pathway analysis in a JMJD3 knockdown human monocytic cell line. |
| المؤلفون: |
Das, Nando Dulal1, Jung, Kyoung Hwa1, Choi, Mi Ran1, Yoon, Hyun Soo2, Kim, Seung Hyun2, Chai, Young Gyu1 |
| المصدر: |
Cell Biochemistry & Function. Apr2012, Vol. 30 Issue 3, p224-232. 9p. |
| مستخلص: |
JMJD3, a Jumonji C family histone demethylase, is induced by transcription factor, nuclear factor-kappa B (NF- κB), in response to various stimuli. JMJD3 is crucial for erasing histone-3 lysine-27 trimethylation (H3K27me3), a modification associated with transcriptional repression and is responsible for the activation of a diverse set of genes. Here, we identify the genes in human leukaemia monocyte (THP-1) human monocytic cells that are significantly affected by the stable knockdown (kd) of JMJD3. Global gene expression levels were detected in stable JMJD3 knockdown THP-1 cells and in tumor necrosis factor-alpha (TNF-α)-stimulated JMJD3-kd THP-1 cells by using a 12-plex NimbleGen human whole genome array. In addition, datasets were analysed by using Ingenuity Pathway Analysis. Stable knockdown of JMJD3 in THP-1 cells affected particularly in expression levels and in downstream effects on inflammatory signalling pathways. JMJD3 attenuation down-regulates various key genes in NF-κB, chemokine and CD40 signalling, and mostly affects inflammatory disease response molecules. In addition, chromatin immunoprecipitation revealed that JMJD3-kd could inhibit several NF- κB-regulated inflammatory genes by recruiting repressive histone-3 lysine-27 trimethylation to their promoters. Moreover, this study significantly highlights the connexion of NF- κB with JMJD3, which suggests an epigenetic regulation in different signalling pathways. Finally, this study establishes novel JMJD3 targets through Ingenuity Pathway Analysis. Copyright © 2012 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR] |
| قاعدة البيانات: |
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