ArticleThe EMBO journal2014
Akirin specifies NF-κB selectivity of Drosophila innate immune response via chromatin remodeling.
Article in The EMBO journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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57 citing papers in PubMed, 101 citations in OpenAlex.
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- A U3 snoRNA is required for the regulation of chromatin dynamics and antiviral response in Drosophila melanogaster.Nucleic acids research · 2025Article
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- Subunits Med12 and Med13 of Mediator Cooperate with Subunits SAYP and Bap170 of SWI/SNF in Active Transcription inInternational journal of molecular sciences · 2024Article
- Role of nuclear protein Akirin in the modulation of female reproduction inFrontiers in physiology · 2024Article
- High-fat diets induce inflammatory IMD/NFκB signaling via gut microbiota remodeling inFrontiers in cellular and infection microbiology · 2024Article
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- Dynamic Regulation of NF-κB Response in Innate Immunity: The Case of the IMD Pathway in Drosophila.Biomedicines · 2022Review
- Transcriptional Repression of Aerobic Glycolysis by OVOL2 in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
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- Protein Phosphatase 4 Negatively Regulates the Immune Deficiency-NF-κB Pathway during theJournal of immunology (Baltimore, Md. : 1950) · 2021Article
- Rapid Genomic Evolution Drives the Diversification of Male Reproductive Genes in Dung Beetles.Genome biology and evolution · 2021Article
- Drosophila H2Av negatively regulates the activity of the IMD pathway via facilitating Relish SUMOylation.PLoS genetics · 2021Article
- Verloren negatively regulates the expression of IMD pathway dependent antimicrobial peptides in Drosophila.Scientific reports · 2021Article
- Function of cofactor Akirin2 in the regulation of gene expression in model human Caucasian neutrophil-like HL60 cells.Bioscience reports · 2021Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The network of NF-κB-dependent transcription that activates both pro- and anti-inflammatory genes in mammals is still unclear. As NF-κB factors are evolutionarily conserved, we used Drosophila to understand this network. The NF-κB transcription factor Relish activates effector gene expression following Gram-negative bacterial immune challenge. Here, we show, using a genome-wide approach, that the conserved nuclear protein Akirin is a NF-κB co-factor required for the activation of a subset of Relish-dependent genes correlating with the presence of H3K4ac epigenetic marks. A large-scale unbiased proteomic analysis revealed that Akirin orchestrates NF-κB transcriptional selectivity through the recruitment of the Osa-containing-SWI/SNF-like Brahma complex (BAP). Immune challenge in Drosophila shows that Akirin is required for the transcription of a subset of effector genes, but dispensable for the transcription of genes that are negative regulators of the innate immune response. Therefore, Akirins act as molecular selectors specifying the choice between subsets of NF-κB target genes. The discovery of this mechanism, conserved in mammals, paves the way for the establishment of more specific and less toxic anti-inflammatory drugs targeting pro-inflammatory genes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.