ArticleNature genetics2015
Early enhancer establishment and regulatory locus complexity shape transcriptional programs in hematopoietic differentiation.
Article in Nature genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
58 citing papers in PubMed.
- Tissue-Specific Chromatin Accessibility Regions and Transcription Factor Binding Sites in Pig Brain and Endocrine Tissues.Molecular neurobiology · 2025Article
- Understanding and reversing mammary tumor-driven reprogramming of myelopoiesis to reduce metastatic spread.Cancer cell · 2025Article
- Perspective on recent developments and challenges in regulatory and systems genomics.Bioinformatics advances · 2025Review
- Editorial: Epigenetics and genomic causality in development and chromatin research.Frontiers in epigenetics and epigenomics · 2025Article
- Single-cell analysis of chromatin and expression reveals age- and sex-associated alterations in the human heart.Communications biology · 2024Article
- Quantifying cell-state densities in single-cell phenotypic landscapes using Mellon.Nature methods · 2024Article
- SEACells infers transcriptional and epigenomic cellular states from single-cell genomics data.Nature biotechnology · 2023Article
- Oncogenic K-Ras suppresses global miRNA function.Molecular cell · 2023Article
- Quantifying Cell-State Densities in Single-Cell Phenotypic Landscapes using Mellon.bioRxiv : the preprint server for biology · 2023Article
- SeATAC: a tool for exploring the chromatin landscape and the role of pioneer factors.Genome biology · 2023Article
- Functional inference of gene regulation using single-cell multi-omics.Cell genomics · 2022Article
- Changes in chromatin accessibility are not concordant with transcriptional changes for single-factor perturbations.Molecular systems biology · 2022Article
- Phenotypic heterogeneity driven by plasticity of the intermediate EMT state governs disease progression and metastasis in breast cancer.Science advances · 2022Article
- Predicting which genes will respond to transcription factor perturbations.G3 (Bethesda, Md.) · 2022Article
- Dynamic regulatory module networks for inference of cell type-specific transcriptional networks.Genome research · 2022Article
- Extended intergenic DNA contributes to neuron-specific expression of neighboring genes in the mammalian nervous system.Nature communications · 2022Article
- Chromatin interaction-aware gene regulatory modeling with graph attention networks.Genome research · 2022Article
- Article
- Artificial intelligence in cancer research, diagnosis and therapy.Nature reviews. Cancer · 2021Article
- Discrete regulatory modules instruct hematopoietic lineage commitment and differentiation.Nature communications · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
We carried out an integrative analysis of enhancer landscape and gene expression dynamics during hematopoietic differentiation using DNase-seq, histone mark ChIP-seq and RNA sequencing to model how the early establishment of enhancers and regulatory locus complexity govern gene expression changes at cell state transitions. We found that high-complexity genes-those with a large total number of DNase-mapped enhancers across the lineage-differ architecturally and functionally from low-complexity genes, achieve larger expression changes and are enriched for both cell type-specific and transition enhancers, which are established in hematopoietic stem and progenitor cells and maintained in one differentiated cell fate but lost in others. We then developed a quantitative model to accurately predict gene expression changes from the DNA sequence content and lineage history of active enhancers. Our method suggests a new mechanistic role for PU.1 at transition peaks during B cell specification and can be used to correct assignments of enhancers to genes.
Indexed as
Identifiers
What OpenQuestion holds
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.