ArticleCell death & disease2019
The Cornelia de Lange Syndrome-associated factor NIPBL interacts with BRD4 ET domain for transcription control of a common set of genes.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- NIPBL-mediated 3D genome folding translates enhancer priming into gene activation and safeguards lineage fidelity during embryonic transitions.bioRxiv : the preprint server for biology · 2025Article
- A Cornelia de Lange syndrome NIPBL 5'-UTR mutation reduces cell proliferation in anBiomedical reports · 2025Article
- Non-Classic Cornelia de Lange Syndrome Due toChildren (Basel, Switzerland) · 2025Review
- Transcription factors form a ternary complex with NIPBL/MAU2 to localize cohesin at enhancers.Nucleic acids research · 2025Article
- ANKRD11 binding to cohesin suggests a connection between KBG syndrome and Cornelia de Lange syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The chromatin tapestry as a framework for neurodevelopment.Genome research · 2024Review
- The NIPBL-gene mutation of a Cornelia de Lange Syndrome patient causes deficits in the hepatocyte differentiation of induced Pluripotent Stem Cells via altered chromatin-accessibility.Cellular and molecular life sciences : CMLS · 2024Article
- Stepwise de novo establishment of inactive X chromosome architecture in early development.Nature genetics · 2024Article
- BRD2 promotes antibody class switch recombination by facilitating DNA repair in collaboration with NIPBL.Nucleic acids research · 2024Article
- BRD4 binds to active cranial neural crest enhancers to regulate RUNX2 activity during osteoblast differentiation.Development (Cambridge, England) · 2024Article
- High-sensitive nascent transcript sequencing reveals BRD4-specific control of widespread enhancer and target gene transcription.Nature communications · 2023Article
- Epigenetic Reader Bromodomain-Containing Protein 4 in Aging-Related Vascular Pathologies and Diseases: Molecular Basis, Functional Relevance, and Clinical Potential.Biomolecules · 2023Review
- 3D enhancer-promoter interactions and multi-connected hubs: Organizational principles and functional roles.Cell reports · 2023Review
- Transcription shapes 3D chromatin organization by interacting with loop extrusion.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Different NIPBL requirements of cohesin-STAG1 and cohesin-STAG2.Nature communications · 2023Article
- Bromodomain and Extra-Terminal Proteins in Brain Physiology and Pathology: BET-ing on Epigenetic Regulation.Biomedicines · 2023Review
- Cohesin regulates alternative splicing.Science advances · 2023Article
- The Green Valley ofCells · 2022Review
- Dicer promotes genome stability via the bromodomain transcriptional co-activator BRD4.Nature communications · 2022Article
- Genetically induced redox stress occurs in a yeast model for Roberts syndrome.G3 (Bethesda, Md.) · 2022Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in NIPBL are the major cause of Cornelia de Lange Syndrome (CdLS). NIPBL is the cohesin-loading factor and has recently been associated with the BET (bromodomains and extra-terminal (ET) domain) proteins BRD2 and BRD4. Related to this, a CdLS-like phenotype has been described associated to BRD4 mutations. Here, we show direct interaction of NIPBL with different BET members in yeast, and selective interaction with BRD4 in cells, being the ET domain involved in the interaction. To understand the relationship between NIPBL and BET proteins, we have performed RNA-Seq expression analysis following depletion of the different proteins. Results indicate that genes regulated by NIPBL largely overlap with those regulated by BRD4 but not with those regulated by BRD2. ChIP-Seq analysis indicates preferential NIPBL occupancy at promoters, and knockdown experiments show mutual stabilization of NIPBL and BRD4 on co-regulated promoters. Moreover, human fibroblasts from CdLS probands with mutations in NIPBL show reduced BRD4 at co-occupied promoters. Functional analysis in vivo, using mutants of Drosophila melanogaster, confirmed the genetic interaction between Nipped-B and fs(1)h, the orthologs of human NIPBL and BRD4, respectively. Thus, we provide evidence for NIPBL and BRD4 cooperation in transcriptional regulation, which should contribute to explain the recently observed CdLS-like phenotype associated with BRD4 mutations.
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