ArticleMolecular cell2021
ZNF410 Uniquely Activates the NuRD Component CHD4 to Silence Fetal Hemoglobin Expression.
Article in Molecular cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 2 of them syntheses that pooled it.
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Who cites it
56 citing papers in PubMed, 2 syntheses or guidelines pooled it, 83 citations in OpenAlex.
- Meta-analysis of integrated ChIP-seq and transcriptome data revealed genomic regions affected by estrogen receptor alpha in breast cancer.BMC medical genomics · 2023Pooled it
- Using Clustered Regularly Interspaced Short Palindromic Repeats gene editing to induce permanent expression of fetal hemoglobin in β-thalassemia and sickle cell disease: A comparative meta-analysis.Frontiers in medicine · 2022Pooled it
- MBNL1 hijacks a structured single-stranded distal DNA element to sustainScience advances · 2026Article
- Motif-Cluster: Motif driven prioritization of transcription factor binding clusters.PLoS computational biology · 2026Article
- PGC-1α agonism via oral administration of ZLN005 induces fetal hemoglobin and is antisickling in sickle mice.Blood advances · 2026Article
- Bipartite DNA binding domain of transcription factor BCL11B binds clustered short DNA sequence motifs.bioRxiv : the preprint server for biology · 2026Article
- Dissecting polycomb complexes for enhanced fetal hemoglobin production.bioRxiv : the preprint server for biology · 2026Article
- Genome-Wide Association Studies for 24 Hematological Traits in Production Pigs Before and After Weaning.Animal genetics · 2026Article
- Regulation of BCL11A DNA binding and expression in human erythrocyte precursor HUDEP-2 cells.bioRxiv : the preprint server for biology · 2026Article
- Investigate the Effect of ZFP64 on mRNA Expression of HBG Based on Bioinformatics and Experimental Validation.Cell biochemistry and biophysics · 2025Article
- Mechanisms of Globin Gene Regulation in Mammals.Annual review of genetics · 2025Review
- Removal of promoter CpG methylation by epigenome editing reverses HBG silencing.Nature communications · 2025Article
- Multimeric transcription factor BCL11A utilizes two zinc-finger tandem arrays to bind clustered short sequence motifs.Nature communications · 2025Article
- FLT1 and other candidate fetal haemoglobin modifying loci in sickle cell disease in African ancestries.Nature communications · 2025Article
- MYB represses ζ-globin expression through upregulating ETO2.Acta biochimica et biophysica Sinica · 2025Article
- Putative looping factor ZNF143/ZFP143 is an essential transcriptional regulator with no looping function.Molecular cell · 2025Article
- The molecular mechanism and utilization of ZmMs7-mediated dominant nuclear sterility inFrontiers in plant science · 2025Article
- ZNF512B binds RBBP4 via a variant NuRD interaction motif and aggregates chromatin in a NuRD complex-independent manner.Nucleic acids research · 2024Article
- Review
- Updated understanding of the protein-DNA recognition code used by C2H2 zinc finger proteins.Current opinion in structural biology · 2024Review
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Authors and funding
20 authors at 7 institutions in 2 countries.
Funding
Abstract
Metazoan transcription factors typically regulate large numbers of genes. Here we identify via a CRISPR-Cas9 genetic screen ZNF410, a pentadactyl DNA-binding protein that in human erythroid cells directly activates only a single gene, the NuRD component CHD4. Specificity is conveyed by two highly evolutionarily conserved clusters of ZNF410 binding sites near the CHD4 gene with no counterparts elsewhere in the genome. Loss of ZNF410 in adult-type human erythroid cell culture systems and xenotransplantation settings diminishes CHD4 levels and derepresses the fetal hemoglobin genes. While previously known to be silenced by CHD4, the fetal globin genes are exposed here as among the most sensitive to reduced CHD4 levels.. In vitro DNA binding assays and crystallographic studies reveal the ZNF410-DNA binding mode. ZNF410 is a remarkably selective transcriptional activator in erythroid cells, and its perturbation might offer new opportunities for treatment of hemoglobinopathies.
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