ArticleDevelopment (Cambridge, England)2014
Sall1 balances self-renewal and differentiation of renal progenitor cells.
Article in Development (Cambridge, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed.
- A Circuit of Mechanically Regulated Transcription Factors Balances Regenerative and Fibrotic Memory of Mesenchymal Stromal Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Dose-Dependent and Non-Autonomous Signaling in CAKUT: A Lineage-Specific Framework from Conditional Knockout Studies.Biomolecules · 2026Review
- Genetic and embryonic transcriptome analyses reveal the molecular and developmental basis of Mayer-Rokitansky-Küster-Hauser syndrome.Journal of medical genetics · 2026Article
- Transcription factors ETV4 and ETV5 are required for nephron progenitor cell maintenance, distal nephron development and connection to the collecting system.Frontiers in cell and developmental biology · 2026Article
- Generation of exogenous kidneys via CRISPR/Cas9 mediated blastocyst complementation targeting Osr1 gene in mice.Scientific reports · 2025Article
- SALL1 Is an Orchestrator of Uterine Receptivity in Part via Titration of Estrogen Signaling.Endocrinology · 2025Article
- Transcription factors that define the epigenome structures and transcriptomes in microglia.Experimental hematology · 2025Review
- Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Nephron progenitor fate is modulated by angiotensin type 1 receptor signaling in human kidney organoids.Stem cells (Dayton, Ohio) · 2025Article
- A novel SALL1 C757T mutation in a Chinese family causes a rare disease --Townes-Brocks syndrome.Italian journal of pediatrics · 2024Article
- Long-term expandable mouse and human-induced nephron progenitor cells enable kidney organoid maturation and modeling of plasticity and disease.Cell stem cell · 2024Article
- Shared features in ear and kidney development - implications for oto-renal syndromes.Disease models & mechanisms · 2024Article
- Altered binding affinity of SIX1-Q177R correlates with enhanced WNT5A and WNT pathway effector expression in Wilms tumor.Disease models & mechanisms · 2023Article
- Identification of two novel SALL1 mutations in chinese families with townes-brocks syndrome and literature review.Orphanet journal of rare diseases · 2023Review
- Targeting the ADPKD methylome using nanoparticle-mediated combination therapy.APL bioengineering · 2023Article
- Principles of human and mouse nephron development.Nature reviews. Nephrology · 2022Review
- A scalable organoid model of human autosomal dominant polycystic kidney disease for disease mechanism and drug discovery.Cell stem cell · 2022Article
- Spatial transcriptional mapping of the human nephrogenic program.Developmental cell · 2021Article
- The core SWI/SNF catalytic subunit Brg1 regulates nephron progenitor cell proliferation and differentiation.Developmental biology · 2020Article
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Authors and funding
5 authors.
Funding
Abstract
The formation of the proper number of functional nephrons requires a delicate balance between renal progenitor cell self-renewal and differentiation. The molecular factors that regulate the dramatic expansion of the progenitor cell pool and differentiation of these cells into nephron precursor structures (renal vesicles) are not well understood. Here we show that Sall1, a nuclear transcription factor, is required to maintain the stemness of nephron progenitor cells. Transcriptional profiling of Sall1 mutant cells revealed a striking pattern, marked by the reduction of progenitor genes and amplified expression of renal vesicle differentiation genes. These global changes in gene expression were accompanied by ectopic differentiation at E12.5 and depletion of Six2+Cited1+ cap mesenchyme progenitor cells. These findings highlight a novel role for Sall1 in maintaining the stemness of the progenitor cell pool by restraining their differentiation into renal vesicles.
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