Observational studyNature communications2021
Genetic perturbation of PU.1 binding and chromatin looping at neutrophil enhancers associates with autoimmune disease.
Observational study in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
34 citing papers in PubMed, 72 citations in OpenAlex.
- Review
- Engineered Neutrophils in Translational Medicine: Gene Editing, Nanotechnology, and AI-Driven Clinical Breakthroughs.Advanced healthcare materials · 2026Review
- Multitissue, multi-time point transcriptomic atlas of aging in mice and rats.Science advances · 2026Article
- Shaping neutrophil morphology and function: the importance of a segmented nucleus.Nature reviews. Immunology · 2026Review
- The Predictive Value of Neutrophil Extracellular Trap-Related Risk Score in Prognosis and Immune Microenvironment of Colorectal Cancer Patients.Molecular biotechnology · 2025Article
- Article
- Article
- Genetic coupling of enhancer activity and connectivity in gene expression control.Nature communications · 2025Article
- Chromatin changes associated with neutrophil extracellular trap formation in whole blood reflect complex immune signaling.Frontiers in immunology · 2025Article
- Redistribution of PU.1 partner transcription factor RUNX1 binding secures cell survival during leukemogenesis.The EMBO journal · 2024Article
- Robust estimation of cancer and immune cell-type proportions from bulk tumor ATAC-Seq data.eLife · 2024Article
- Identifying genetic variants associated with chromatin looping and genome function.Nature communications · 2024Article
- Non-coding variants impact cis-regulatory coordination in a cell type-specific manner.Genome biology · 2024Article
- Reprogramming of 3D genome structure underlying HSPC development in zebrafish.Stem cell research & therapy · 2024Article
- Evolutionary dynamics of tipifarnib in HRAS mutated head and neck squamous cell carcinoma.Oral oncology · 2024Article
- Hi-C, a chromatin 3D structure technique advancing the functional genomics of immune cells.Frontiers in genetics · 2024Review
- Translation of genome-wide association study: from genomic signals to biological insights.Frontiers in genetics · 2024Review
- Transcription factor-binding k-mer analysis clarifies the cell type dependency of binding specificities and cis-regulatory SNPs in humans.BMC genomics · 2023Article
- Blood cell traits' GWAS loci colocalization with variation in PU.1 genomic occupancy prioritizes causal noncoding regulatory variants.Cell genomics · 2023Article
- Understanding the evolution of immune genes in jawed vertebrates.Journal of evolutionary biology · 2023Review
Corrections and comments
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Authors and funding
27 authors at 8 institutions in 5 countries.
Funding
Abstract
Neutrophils play fundamental roles in innate immune response, shape adaptive immunity, and are a potentially causal cell type underpinning genetic associations with immune system traits and diseases. Here, we profile the binding of myeloid master regulator PU.1 in primary neutrophils across nearly a hundred volunteers. We show that variants associated with differential PU.1 binding underlie genetically-driven differences in cell count and susceptibility to autoimmune and inflammatory diseases. We integrate these results with other multi-individual genomic readouts, revealing coordinated effects of PU.1 binding variants on the local chromatin state, enhancer-promoter contacts and downstream gene expression, and providing a functional interpretation for 27 genes underlying immune traits. Collectively, these results demonstrate the functional role of PU.1 and its target enhancers in neutrophil transcriptional control and immune disease susceptibility.
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Registered trials
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.