ArticleDiabetologia2015
SOX4 cooperates with neurogenin 3 to regulate endocrine pancreas formation in mouse models.
Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 37 citations in OpenAlex.
- Resolving human α versus β cell fate allocation for the generation of stem cell-derived islets.Nature communications · 2026Article
- Genome-wide cell type-specific and sex-specific transcriptional dysregulation in the islet of Langerhans underlies islet dysfunction in Down syndrome-related diabetes.bioRxiv : the preprint server for biology · 2026Article
- Bridging pancreatic and hepatic development: overlapping genes and their role in diabetes.Cellular & molecular biology letters · 2025Review
- Activation of human endogenous retroviruses by Sox proteins induces cell apoptosis via the caspase-3 pathway.Frontiers in microbiology · 2025Article
- Identification of mouse and human embryonic pancreatic cells with adult ProcrFrontiers in endocrinology · 2025Article
- Identification of genes related to fatty acid metabolism in type 2 diabetes mellitus.Biochemistry and biophysics reports · 2024Article
- Transcriptional coactivator MED15 is required for beta cell maturation.Nature communications · 2024Article
- Human stomach tissue as alternative source of insulin-producing cells.Nature reviews. Endocrinology · 2023Article
- Type 2 diabetes susceptibility gene GRK5 regulates physiological pancreatic β-cell proliferation via phosphorylation of HDAC5.iScience · 2023Article
- Article
- Role of the Transcription Factor MAFA in the Maintenance of Pancreatic β-Cells.International journal of molecular sciences · 2022Review
- Identification of Novel Regulatory Regions Induced by Intrauterine Growth Restriction in Rat Islets.Endocrinology · 2022Article
- SOX4 promotes high-glucose-induced inflammation and angiogenesis of retinal endothelial cells by activating NF-κB signaling pathway.Open life sciences · 2022Article
- Insights into pancreatic islet cell dysfunction from type 2 diabetes mellitus genetics.Nature reviews. Endocrinology · 2020Review
- Single-Cell Transcriptome Profiling of Mouse and hESC-Derived Pancreatic Progenitors.Stem cell reports · 2018Article
- Functional characteristics of novel pancreatic Pax6 regulatory elements.Human molecular genetics · 2018Article
- Phosphorylation of NEUROG3 Links Endocrine Differentiation to the Cell Cycle in Pancreatic Progenitors.Developmental cell · 2017Article
- Molecular mechanisms of Sox transcription factors during the development of liver, bile duct, and pancreas.Seminars in cell & developmental biology · 2017Review
- Pairing-up SOX to kick-start beta cell genesis.Diabetologia · 2015Article
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7 authors at 2 institutions in 1 country.
Funding
Abstract
aims/hypothesisThe sex-determining region Y (SRY)-related high mobility group (HMG) box (SOX) family of transcription factors is essential for normal organismal development. Despite the longstanding knowledge that many SOX family members are expressed during pancreas development, a role for many of these factors in the establishment of insulin-producing beta cell fate remains to be determined. The aim of this study is to elucidate the role of SOX4 during beta cell development.
methodsWe used pancreas and endocrine progenitor mouse knockouts of Sox4 to uncover the roles of SOX4 during pancreas development. Lineage tracing and in vitro models were used to determine how SOX4 regulates beta cell formation and understand the fate of Sox4-null endocrine lineage cells.
resultsThis study demonstrates a progenitor cell-autonomous role for SOX4 in regulating the genesis of beta cells and shows that it is required at multiple stages of the process. SOX4 deletion in the multipotent pancreatic progenitors resulted in impaired endocrine progenitor cell differentiation. Deletion of SOX4 later in the Neurog3-expressing cells also caused reductions in beta cells. Lineage studies showed loss of Sox4 in endocrine progenitors resulted in a block in terminal islet cell differentiation that was attributed to reduction in the production of key beta cell specification factors. CONCLUSIONS/
interpretationThese results demonstrate that SOX4 is essential for normal endocrine pancreas development both concomitant with, and downstream of, the endocrine fate decision. In conclusion, these studies position Sox4 temporally in the endocrine differentiation programme and provide a new target for improving in vitro differentiation of glucose-responsive pancreatic beta cells.
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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.