ArticleDevelopment (Cambridge, England)2016
Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex.
Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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.
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Who cites it
44 citing papers in PubMed, 89 citations in OpenAlex.
- Article
- Dual genomic localizations and gene regulatory functions of MBD-2 with and without NuRD in Caenorhabditis elegans which lacks DNA methylation.Nature communications · 2026Article
- Neural crest induction requires SALL4-mediated BAF recruitment to lineage specific enhancers.Development (Cambridge, England) · 2025Article
- Zebrafish sall1a and sall4 contribute to body elongation.Developmental biology · 2025Article
- A de novo SALL4 mutation causes unilateral renal agenesis by misregulating genes involved in kidney development.Orphanet journal of rare diseases · 2025Article
- A function of Spalt proteins in heterochromatin organization and maintenance of genomic DNA integrity.Development (Cambridge, England) · 2025Article
- Thalidomide-induced limb malformations: an update and reevaluation.Archives of toxicology · 2025Review
- The enhancer module of Integrator controls cell identity and early neural fate commitment.Nature cell biology · 2025Article
- Mouse and human embryonic genome activation initiate at the one-cell stage.Frontiers in cell and developmental biology · 2025Article
- Reconstitution of pluripotency from mouse fibroblast through Sall4 overexpression.Nature communications · 2024Article
- ZNF512B binds RBBP4 via a variant NuRD interaction motif and aggregates chromatin in a NuRD complex-independent manner.Nucleic acids research · 2024Article
- H3K4me1 facilitates promoter-enhancer interactions and gene activation during embryonic stem cell differentiation.Molecular cell · 2024Article
- Sall4 regulates posterior trunk mesoderm development by promoting mesodermal gene expression and repressing neural genes in the mesoderm.Development (Cambridge, England) · 2024Article
- Live-cell three-dimensional single-molecule tracking reveals modulation of enhancer dynamics by NuRD.Nature structural & molecular biology · 2023Article
- Sall4 restricts glycolytic metabolism in limb buds through transcriptional regulation of glycolytic enzyme genes.Developmental biology · 2023Article
- Ultrasensitive proteomics depicted an in-depth landscape for the very early stage of mouse maternal-to-zygotic transition.Journal of pharmaceutical analysis · 2023Article
- Gene silencing dynamics are modulated by transiently active regulatory elements.Molecular cell · 2023Article
- Structure of SALL4 zinc finger domain reveals link between AT-rich DNA binding and Okihiro syndrome.Life science alliance · 2023Article
- Normal embryonic development and neonatal digit regeneration in mice overexpressing a stem cell factor, Sall4.PloS one · 2022Article
- SALL Proteins; Common and Antagonistic Roles in Cancer.Cancers · 2021Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Sall4 is an essential transcription factor for early mammalian development and is frequently overexpressed in cancer. Although it is reported to play an important role in embryonic stem cell (ESC) self-renewal, whether it is an essential pluripotency factor has been disputed. Here, we show that Sall4 is dispensable for mouse ESC pluripotency. Sall4 is an enhancer-binding protein that prevents precocious activation of the neural gene expression programme in ESCs but is not required for maintenance of the pluripotency gene regulatory network. Although a proportion of Sall4 protein physically associates with the Nucleosome Remodelling and Deacetylase (NuRD) complex, Sall4 neither recruits NuRD to chromatin nor influences transcription via NuRD; rather, free Sall4 protein regulates transcription independently of NuRD. We propose a model whereby enhancer binding by Sall4 and other pluripotency-associated transcription factors is responsible for maintaining the balance between transcriptional programmes in pluripotent cells.
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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.