ArticleMolecular and cellular biology2010
Differential roles of Sall4 isoforms in embryonic stem cell pluripotency.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 2 of them syntheses that pooled it.
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
104 citing papers in PubMed, 2 syntheses or guidelines pooled it, 180 citations in OpenAlex.
- Higher expression of SALL4 predicts poor cancer prognosis: A meta-analysis.Cancer biomarkers : section A of Disease markers · 2017Pooled it
- Identification of 19 new risk loci and potential regulatory mechanisms influencing susceptibility to testicular germ cell tumor.Nature genetics · 2017Pooled it
- Neural crest induction requires SALL4-mediated BAF recruitment to lineage specific enhancers.Development (Cambridge, England) · 2025Article
- SALL4 Is Required for YAP1-Dependent Malignant and Regenerative Hepatocyte-to-Cholangiocyte Reprogramming.Cancer research communications · 2025Article
- ADT increases prostate cancer cell invasion via altering AR/SALL4/SOX2-OCT4 stem cell signaling.Cell biology and toxicology · 2025Article
- Thalidomide-induced limb malformations: an update and reevaluation.Archives of toxicology · 2025Review
- Unveiling distinctions between mesenchymal stromal cells and stem cells by single-cell transcriptomic analysis.Heliyon · 2025Article
- Cytoplasmic SALL4-A isoform expression as a diagnostic marker of less aggressive tumor behavior in gastric cancer.World journal of surgical oncology · 2025Article
- Alternative Splicing in the Heart: The Therapeutic Potential of Regulating the Regulators.International journal of molecular sciences · 2024Review
- SALL4 in gastrointestinal tract cancers: upstream and downstream regulatory mechanisms.Molecular medicine (Cambridge, Mass.) · 2024Review
- Single-cell analysis of isoform switching and transposable element expression during preimplantation embryonic development.PLoS biology · 2024Article
- SALL4 upregulates brain-derived neurotrophic factor to mediate Hedgehog signaling to inhibit carboplatin sensitivity in colon adenocarcinoma.Pharmacogenomics · 2024Article
- Co-expression of PADI isoforms during progenitor differentiation enables functional diversity.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Article
- SALL4 promotes angiogenesis in gastric cancer by regulating VEGF expression and targeting SALL4/VEGF pathway inhibits cancer progression.Cancer cell international · 2023Article
- Transcription factors and splice factors - interconnected regulators of stem cell differentiation.Current stem cell reports · 2023Article
- The new advance of SALL4 in cancer: Function, regulation, and implication.Journal of clinical laboratory analysis · 2023Review
- A Simplified and Effective Approach for the Isolation of Small Pluripotent Stem Cells Derived from Human Peripheral Blood.Biomedicines · 2023Article
- Structure of SALL4 zinc finger domain reveals link between AT-rich DNA binding and Okihiro syndrome.Life science alliance · 2023Article
- Article
- Potential application of human SALL4 on oral squamous cell carcinoma.Annals of translational medicine · 2022Article
44 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Murine embryonic stem (ES) cells are defined by continuous self-renewal and pluripotency. A diverse repertoire of protein isoforms arising from alternative splicing is expressed in ES cells without defined biological roles. Sall4, a transcription factor essential for pluripotency, exists as two isoforms (Sall4a and Sall4b). Both isoforms can form homodimers and a heterodimer with each other, and each can interact with Nanog. By genomewide location analysis, we determined that Sall4a and Sall4b have overlapping, but not identical binding sites within the ES cell genome. In addition, Sall4b, but not Sall4a, binds preferentially to highly expressed loci in ES cells. Sall4a and Sall4b binding sites are distinguished by both epigenetic marks at target loci and their clustering with binding sites of other pluripotency factors. When ES cells expressing a single isoform of Sall4 are generated, Sall4b alone could maintain the pluripotent state, although it could not completely suppress all differentiation markers. Sall4a and Sall4b collaborate in maintenance of the pluripotent state but play distinct roles. Our work is novel in establishing such isoform-specific differences in ES 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.