Similar Datasets
Project description:Purpose: The purpose of this study is to identify the genome-wide binding sites for IRF4 interaction partners PU.1, BATF, and JunB in dendritic cells. These ChIP-seq data were integrated with gene expression analysis in IRF4-sufficient and -deficient BMDCs in order to assemble an IRF4 gene regulatory network. Hematopoietic bone marrow progenitors from C57BL/6 mice were differentiated with GM-CSF and IL-4 for 5 days. On day 6, BMDCs were stimulated for 6 hours with 100ng/ml LPS. Fixed chromatin was immunoprecipitated with anti-PU.1, BATF, and JunB antibodies and subjected to high-throughput sequencing. The sequencing data for the input DNA was previously submitted as GSM999807.
2013-12-22 | E-GEOD-52772 | biostudies-arrayexpress
Project description:Purpose: The purpose of this study is to identify the genome-wide binding sites for IRF4 interaction partners PU.1, BATF, and JunB in dendritic cells. These ChIP-seq data were integrated with gene expression analysis in IRF4-sufficient and -deficient BMDCs in order to assemble an IRF4 gene regulatory network.
2013-12-22 | GSE52772 | GEO
Project description:This study is designed to determine the direct target genes of JunB transcription factor in human keratinocytes Mice with epidermal deletion of JunB transcription factor displayed a psoriasis-like inflammation. The relevance of these findings to humans and the mechanisms mediating JunB function are not fully understood. Here, we demonstrate that impaired JunB function via gene silencing or overexpression of a dominant negative mutant increased human keratinocyte cell proliferation but decreased cell barrier function. RNA-seq revealed over 500 genes affected by JunB loss-of-function which included an upregulation of an array of proinflammatory molecules relevant to psoriasis. Among these were TNFa, CCL2, CXCL10, IL6R and SQSTM1, an adaptor protein involved in NF-kB activation. ChIP-Seq and gene reporter analyses showed that JunB directly suppressed SQSTM1 through binding to a consensus AP-1 cis-element located around 2 Kb upstream of SQSTM1-trasncription start site. Similar to JunB loss-of-function, SQSTM1-overexpression induced TNFa, CCL2 and CXCL10. Conversely, NF-kB-inhibition genetically with a mutant IkBa or pharmacologically with PDTC prevented cytokine, but not IL6R, induction by JunB-deficiency. Taken together, our findings indicate that JunB controls epidermal growth, barrier formation and proinflammatory responses through direct and indirect mechanisms, pinpointing SQSTM1 as a key mediator of JunB-suppression of NF-kB-dependent inflammation.
2015-10-05 | GSE63080 | GEO
Project description:To address the role of JUNB in cell proliferation, we investigated the consequences of JUNB depletion using U2OS human bone osteosarcoma cells. We used microarrays to detail the programme of JUNB dependent gene expression underlying cell proliferation and identified distinct classes of up and down-regulated genes during this process.
2022-09-29 | GSE195987 | GEO
Project description:In order to identify sites bound by c-Jun/JunB in ALK+ ALCL, we performed ChIP-Seq on the Karpas 299 ALK+ ALCL cell line.
2020-09-01 | GSE151413 | GEO
Project description:We performed SMAD2/3 ChIP-seq analysis in MCF10A MII cells. To validate whether the changes in SMAD2/3 binding to the genome indeed resulted in changes in target gene expression, we performed RNA-seq transcriptome analysis after short and long periods of TGFβ stimulation (0, 1.5h and 16h) in MII cells. In addition, we revealed that JUNB is a critical AP1 component for SMAD2/3 binding after TGFβ stimulation. To assess the significance of JUNB for TGFβ-SMAD-target genes on a genome-wide scale, we also performed RNA-seq transcriptome analysis in JUNB-knock-downed MII cells.
2017-11-15 | GSE83786 | GEO
Project description:The human osteosarcoma cell line U2OS contains a functional circadian clock but expresses only a few rhythmic genes. We identified by ChIP-seq analysis 3040 binding sites of the circadian transcription factors BMAL1, CLOCK, and CRY1 in the genome of U2OS cells, comparable to the number found in highly rhythmic tissues like liver.
2016-02-11 | GSE44236 | GEO
Project description:To determne JunB target gene in human keratincoytes Mice with epidermal deletion of JunB transcription factor displayed a psoriasis-like inflammation. The relevance of these findings to humans and the mechanisms mediating JunB function are not fully understood. Here, we demonstrate that impaired JunB function via gene silencing or overexpression of a dominant negative mutant increased human keratinocyte cell proliferation but decreased cell barrier function. RNA-seq revealed over 500 genes affected by JunB loss-of-function which included an upregulation of an array of proinflammatory molecules relevant to psoriasis. Among these were TNFa, CCL2, CXCL10, IL6R and SQSTM1, an adaptor protein involved in NF-kB activation. ChIP-Seq and gene reporter analyses showed that JunB directly suppressed SQSTM1 through binding to a consensus AP-1 cis-element located around 2 Kb upstream of SQSTM1-trasncription start site. Similar to JunB loss-of-function, SQSTM1-overexpression induced TNFa, CCL2 and CXCL10. Conversely, NF-kB-inhibition genetically with a mutant IkBa or pharmacologically with PDTC prevented cytokine, but not IL6R, induction by JunB-deficiency. Taken together, our findings indicate that JunB controls epidermal growth, barrier formation and proinflammatory responses through direct and indirect mechanisms, pinpointing SQSTM1 as a key mediator of JunB-suppression of NF-kB-dependent inflammation.
2015-10-05 | GSE63079 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE21769: Genome wide expression analysis of ER alpha and beta with or without E2 treatment in U2OS cell line. GSE21770: Genome-wide maps of ER beta binding sites in U2OS cells Refer to individual Series
2010-05-11 | E-GEOD-21790 | biostudies-arrayexpress
Project description:To understand molecular mechanisms by which JunB regulates Th17 differentiation, we performed ChIP-seq analyses of JunB-deficient and control Th17 cells.
2017-04-11 | GSE86535 | GEO