ArticleBMC systems biology2013
JunD/AP1 regulatory network analysis during macrophage activation in a rat model of crescentic glomerulonephritis.
Article in BMC systems biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- B cell function in patients with systemic lupus erythematosus is regulated by the upregulation of JunD.Heliyon · 2024Article
- Cis-regulatory interfaces reveal the molecular mechanisms underlying the notochord gene regulatory network of Ciona.Nature communications · 2024Article
- A Common Functional Variant at the Enhancer of the Rheumatoid Arthritis Risk GenePhenomics (Cham, Switzerland) · 2023Article
- Translocator protein is a marker of activated microglia in rodent models but not human neurodegenerative diseases.Nature communications · 2023Article
- PPIP5K2 and PCSK1 are Candidate Genetic Contributors to Familial Keratoconus.Scientific reports · 2019Article
- Vitamin DEBioMedicine · 2019Article
- A Bayesian Approach for Analysis of Whole-Genome Bisulfite Sequencing Data Identifies Disease-Associated Changes in DNA Methylation.Genetics · 2017Article
- Transcriptional and epigenetic substrates of methamphetamine addiction and withdrawal: evidence from a long-access self-administration model in the rat.Molecular neurobiology · 2015Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundFunction and efficiency of a transcription factor (TF) are often modulated by interactions with other proteins or TFs to achieve finely tuned regulation of target genes. However, complex TF interactions are often not taken into account to identify functionally active TF-targets and characterize their regulatory network. Here, we have developed a computational framework for integrated analysis of genome-wide ChIP-seq and gene expression data to identify the functional interacting partners of a TF and characterize the TF-driven regulatory network. We have applied this methodology in a rat model of macrophage dependent crescentic glomerulonephritis (Crgn) where we have previously identified JunD as a TF gene responsible for enhanced macrophage activation associated with susceptibility to Crgn in the Wistar-Kyoto (WKY) strain.
resultsTo evaluate the regulatory effects of JunD on its target genes, we analysed data from two rat strains (WKY and WKY.LCrgn2) that show 20-fold difference in their JunD expression in macrophages. We identified 36 TFs interacting with JunD/Jun and JunD/ATF complexes (i.e., AP1 complex), which resulted in strain-dependent gene expression regulation of 1,274 target genes in macrophages. After lipopolysaccharide (LPS) stimulation we found that 2.4 fold more JunD/ATF-target genes were up-regulated as compared with JunD/Jun-target genes. The enriched 314 genes up-regulated by AP1 complex during LPS stimulation were most significantly enriched for immune response (P = 6.9 × 10⁻⁴) and antigen processing and presentation functions (P = 2.4 × 10⁻⁵), suggesting a role for these genes in macrophage LPS-stimulated activation driven by JunD interaction with Jun/ATF.
conclusionsIn summary, our integrated analyses revealed a large network of TFs interacting with JunD and their regulated targets. Our data also suggest a previously unappreciated contribution of the ATF complex to JunD-mediated mechanisms of macrophage activation in a rat model of crescentic glomerulonephritis.
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