ArticleExperimental hematology2015
Sall4 overexpression blocks murine hematopoiesis in a dose-dependent manner.
Article in Experimental hematology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 20 citations in OpenAlex.
- Review
- SALL4 in gastrointestinal tract cancers: upstream and downstream regulatory mechanisms.Molecular medicine (Cambridge, Mass.) · 2024Review
- Combinatorial genetics reveals the Dock1-Rac2 axis as a potential target for the treatment of NPM1;Cohesin mutated AML.Leukemia · 2022Article
- SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance.International journal of molecular sciences · 2022Review
- FBXO38 Ubiquitin Ligase Controls Sertoli Cell Maturation.Frontiers in cell and developmental biology · 2022Article
- The Interplay between Transcription Factor SALL4 and Histone Modifiers in Hematopoietic Stem and Progenitor Cells.Journal of cellular immunology · 2021Article
- Enhancement of mouse hematopoietic stem/progenitor cell function via transient gene delivery using integration-deficient lentiviral vectors.Experimental hematology · 2018Article
- SALL4 as a transcriptional and epigenetic regulator in normal and leukemic hematopoiesis.Biomarker research · 2018Review
- SALL4 suppresses PTEN expression to promote glioma cell proliferation via PI3K/AKT signaling pathway.Journal of neuro-oncology · 2017Article
- Dynamic Protein Interactions of the Polycomb Repressive Complex 2 during Differentiation of Pluripotent Cells.Molecular & cellular proteomics : MCP · 2016Article
- Ex-vivo expansion of nonhuman primate CD34Stem cell research & therapy · 2016Article
- Optimizing autologous cell grafts to improve stem cell gene therapy.Experimental hematology · 2016Review
- The cohesin-associated protein Wapal is required for proper Polycomb-mediated gene silencing.Epigenetics & chromatin · 2016Article
- Human haematopoietic stem/progenitor cells express several functional sex hormone receptors.Journal of cellular and molecular medicine · 2016Article
- Article
- Two missense mutations in SALL4 in a patient with microphthalmia, coloboma, and optic nerve hypoplasia.Ophthalmic geneticsArticle
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Sal-like protein 4 (SALL4) is a transcription factor that exists in two splice isoforms, SALL4a and SALL4b, and regulates transcription in embryonic stem cells, hematopoiesis, and acute myeloid leukemia. Constitutive overexpression of SALL4 in mice induces acute myeloid leukemia. Interestingly, a potential benefit of using SALL4 to facilitate ex vivo hematopoietic stem cell expansion has been proposed. However, distinct roles for how SALL4 contributes to normal versus malignant processes remain undefined. Here we show that SALL4b is the predominant isoform in murine hematopoietic stem cells and progenitors. Overexpression of either SALL4 isoform in hematopoietic stem cells or progenitors impairs hematopoietic colony formation and expansion in vitro. Lineage-negative bone marrow overexpressing SALL4b fails to engraft and reconstitute hematopoiesis when transplanted. We found that both SALL4a and SALL4b overexpression impair hematopoiesis, in part through dose-dependent repression of BMI1. Additionally, we have identified the following potential novel SALL4 target genes in hematopoiesis: ARID5B (SALL4a and SALL4b), EZH2, and KLF2 (SALL4a). Lastly, we found that SALL4 expression is variable in acute myeloid leukemia, ranging from no expression to levels comparable to embryonic stem cells. These results show that SALL4 isoforms contribute to only a subset of acute myeloid leukemia and that overexpression of SALL4 isoforms impairs hematopoiesis through repression of BMI1. Together these data demonstrate the sensitivity of hematopoiesis to appropriately balanced SALL4 expression, highlighting the importance of regulating this dynamic in potential therapeutic applications such as ex vivo stem cell expansion.
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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.