ArticleDisease models & mechanisms2012
Sall1 regulates cortical neurogenesis and laminar fate specification in mice: implications for neural abnormalities in Townes-Brocks syndrome.
Article in Disease models & mechanisms, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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
32 citing papers in PubMed, 43 citations in OpenAlex.
- Townes-Brocks syndrome: genotype-phenotype correlations of SALL1 variants in our series and the literature.European journal of human genetics : EJHG · 2025Article
- SALL1 Is an Orchestrator of Uterine Receptivity in Part via Titration of Estrogen Signaling.Endocrinology · 2025Article
- Identification of Pappa and Sall3 as Gli3 direct target genes acting downstream of cilia signaling in corticogenesis.Cerebral cortex (New York, N.Y. : 1991) · 2024Article
- A Genotyped Case of Townes-Brocks Syndrome with Absent Pulmonary Valve Syndrome from Turkey.Journal of pediatric genetics · 2024Article
- The long noncoding RNA nHOTAIRM1 is necessary for differentiation and activity of iPSC-derived spinal motor neurons.Cell death & disease · 2023Article
- Article
- Microglia-derived CCL2 has a prime role in neocortex neuroinflammation.Fluids and barriers of the CNS · 2022Article
- Identification of microRNAs related with neural germ layer lineage-specific progenitors during reprogramming.Journal of molecular histology · 2022Article
- Massively parallel reporter perturbation assays uncover temporal regulatory architecture during neural differentiation.Nature communications · 2022Article
- Reprogramming of the epigenome in neurodevelopmental disorders.Critical reviews in biochemistry and molecular biology · 2022Review
- Chromatin Remodeling in the Brain-aInternational journal of molecular sciences · 2021Review
- Analysis of homozygous and heterozygous Csf1r knockout in the rat as a model for understanding microglial function in brain development and the impacts of human CSF1R mutations.Neurobiology of disease · 2021Article
- Heterozygous loss of WBP11 function causes multiple congenital defects in humans and mice.Human molecular genetics · 2020Article
- Role of Microglia in Modulating Adult Neurogenesis in Health and Neurodegeneration.International journal of molecular sciences · 2020Review
- Article
- Transcriptional and Epigenetic Regulation of Microglia in Health and Disease.Trends in molecular medicine · 2019Review
- Targeting Microglia and Macrophages: A Potential Treatment Strategy for Multiple Sclerosis.Frontiers in pharmacology · 2019Review
- Loss of IL-10 Promotes Differentiation of Microglia to a M1 Phenotype.Frontiers in cellular neuroscience · 2019Article
- The Role of Neuronal Factors in the Epigenetic Reprogramming of Microglia in the Normal and Diseased Central Nervous System.Frontiers in cellular neuroscience · 2019Review
- Microglial signatures and their role in health and disease.Nature reviews. Neuroscience · 2018Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
Abstract
Progenitor cells in the cerebral cortex undergo dynamic cellular and molecular changes during development. Sall1 is a putative transcription factor that is highly expressed in progenitor cells during development. In humans, the autosomal dominant developmental disorder Townes-Brocks syndrome (TBS) is associated with mutations of the SALL1 gene. TBS is characterized by renal, anal, limb and auditory abnormalities. Although neural deficits have not been recognized as a diagnostic characteristic of the disease, ~10% of patients exhibit neural or behavioral abnormalities. We demonstrate that, in addition to being expressed in peripheral organs, Sall1 is robustly expressed in progenitor cells of the central nervous system in mice. Both classical- and conditional-knockout mouse studies indicate that the cerebral cortex is particularly sensitive to loss of Sall1. In the absence of Sall1, both the surface area and depth of the cerebral cortex were decreased at embryonic day 18.5 (E18.5). These deficiencies are associated with changes in progenitor cell properties during development. In early cortical progenitor cells, Sall1 promotes proliferative over neurogenic division, whereas, at later developmental stages, Sall1 regulates the production and differentiation of intermediate progenitor cells. Furthermore, Sall1 influences the temporal specification of cortical laminae. These findings present novel insights into the function of Sall1 in the developing mouse cortex and provide avenues for future research into potential neural deficits in individuals with TBS.
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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.