Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 채영규 | - |
dc.date.accessioned | 2018-03-08T04:07:51Z | - |
dc.date.available | 2018-03-08T04:07:51Z | - |
dc.date.issued | 2012-04 | - |
dc.identifier.citation | CELL BIOCHEMISTRY AND FUNCTION; APR 2012, 30, 3, p224-p232, 9p. | en_US |
dc.identifier.issn | 0263-6484 | - |
dc.identifier.uri | http://onlinelibrary.wiley.com/doi/10.1002/cbf.1839/abstract | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/43525 | - |
dc.description.abstract | JMJD3, a Jumonji C family histone demethylase, is induced by transcription factor, nuclear factor-kappa B (NF-?B), 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-a)-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-?B, chemokine and CD40 signalling, and mostly affects inflammatory disease response molecules. In addition, chromatin immunoprecipitation revealed that JMJD3-kd could inhibit several NF-?B-regulated inflammatory genes by recruiting repressive histone-3 lysine-27 trimethylation to their promoters. Moreover, this study significantly highlights the connexion of NF-?B with JMJD3, which suggests an epigenetic regulation in different signalling pathways. Finally, this study establishes novel JMJD3 targets through Ingenuity Pathway Analysis. Copyright (C) 2012 John Wiley & Sons, Ltd. | en_US |
dc.description.sponsorship | This project was performed under the Basic Science Research Program (2009-0077023) of the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology, Republic of Korea. | en_US |
dc.language.iso | en | en_US |
dc.publisher | WILEY-BLACKWELL | en_US |
dc.subject | JMJD3 | en_US |
dc.subject | NF-?B | en_US |
dc.subject | THP-1 cells | en_US |
dc.subject | IPA | en_US |
dc.subject | gene networking | en_US |
dc.title | Gene networking and inflammatory pathway analysis in a JMJD3 knockdown human monocytic cell line | en_US |
dc.type | Article | en_US |
dc.relation.no | 3 | - |
dc.relation.volume | 30 | - |
dc.identifier.doi | 0.1002/cbf.1839/abstract | - |
dc.relation.page | 224-232 | - |
dc.relation.journal | CELL BIOCHEMISTRY AND FUNCTION | - |
dc.contributor.googleauthor | Das, Nando | - |
dc.contributor.googleauthor | Jung, Kyoung Hwa | - |
dc.contributor.googleauthor | Choi, Mi Ran | - |
dc.contributor.googleauthor | Chai, Young Gyu | - |
dc.contributor.googleauthor | Yoon, Hyun Soo | - |
dc.contributor.googleauthor | Kim, Seung Hyun | - |
dc.relation.code | 2012201734 | - |
dc.sector.campus | S | - |
dc.sector.daehak | GRADUATE SCHOOL[S] | - |
dc.sector.department | DEPARTMENT OF BIONANOTECHNOLOGY | - |
dc.identifier.pid | ygchai | - |
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