ArticleNature communications2019
Diverse motif ensembles specify non-redundant DNA binding activities of AP-1 family members in macrophages.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 87 citations in OpenAlex.
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- Depletion and replacement of tissue-resident macrophages in mice with germ-line deletion of a conserved enhancer in the Csf1r locus.Development (Cambridge, England) · 2026Article
- YAP/TAZ inhibition refines TGF-β signaling to prevent laryngeal fibrosis.bioRxiv : the preprint server for biology · 2026Article
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- SMARCA4 activation engages FOSL1 to drive enhancer reprogramming and tumorigenic phenotypes in SMARCA4-deficient LUAD cells.Cell death discovery · 2026Article
- Efficient In Vivo Pharmacological Inhibition of ΔFOSB, an AP-1 Transcription Factor, in the Brain.ACS chemical neuroscience · 2026Article
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- The C-reactive protein-triglyceride glucose index (CTI) predicts mortality in cardiovascular-kidney-metabolic syndrome: a dual-cohort study with machine learning validation.International journal of surgery (London, England) · 2026Article
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- Mutant CEBPA promotes tolerance to inflammatory stress through deficient AP-1 activation.Nature communications · 2025Article
- Regulation of developmentally controlled enhancer activity by extrinsic signals in normal and malignant cells: AP-1 at the centre.Frontiers in epigenetics and epigenomics · 2024Article
- TIANA: transcription factors cooperativity inference analysis with neural attention.BMC bioinformatics · 2024Article
- Conservation ofCells · 2024Article
- c-Jun signaling during initial HSV-1 infection modulates latency to enhance later reactivation in addition to directly promoting the progression to full reactivation.Journal of virology · 2024Article
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- c-Jun Signaling During Initial HSV-1 Infection Modulates Latency to Enhance Later Reactivation in addition to Directly Promoting the Progression to Full Reactivation.bioRxiv : the preprint server for biology · 2023Article
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Mechanisms by which members of the AP-1 family of transcription factors play non-redundant biological roles despite recognizing the same DNA sequence remain poorly understood. To address this question, here we investigate the molecular functions and genome-wide DNA binding patterns of AP-1 family members in primary and immortalized mouse macrophages. ChIP-sequencing shows overlapping and distinct binding profiles for each factor that were remodeled following TLR4 ligation. Development of a machine learning approach that jointly weighs hundreds of DNA recognition elements yields dozens of motifs predicted to drive factor-specific binding profiles. Machine learning-based predictions are confirmed by analysis of the effects of mutations in genetically diverse mice and by loss of function experiments. These findings provide evidence that non-redundant genomic locations of different AP-1 family members in macrophages largely result from collaborative interactions with diverse, locus-specific ensembles of transcription factors and suggest a general mechanism for encoding functional specificities of their common recognition motif.
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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.