ArticleDevelopment (Cambridge, England)2013
Sox17 haploinsufficiency results in perinatal biliary atresia and hepatitis in C57BL/6 background mice.
Article in Development (Cambridge, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 68 citations in OpenAlex.
- Two distributed enhancers of Sox17 additively regulate the developmental fate of bipotential ventral pancreato-biliary progenitor cells.Development (Cambridge, England) · 2026Article
- Enhanced Peribiliary Gland Detachment in Aged Donor Grafts After Rat Liver Transplantation.Transplantation direct · 2026Article
- Ability to form Sox17-induced hematopoietic cell clusters varies among distinct hematopoietic sites during development.Inflammation and regeneration · 2026Article
- SOX17 in pulmonary arterial hypertension: from development to clinical phenotype.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Versatile application of fast green FCF as a visible cholangiogram in adult mice to medium-sized mammals.Scientific reports · 2025Article
- Positive autoregulation of Sox17 is necessary for gallbladder and extrahepatic bile duct formation.Development (Cambridge, England) · 2025Article
- Identification of Gallbladder-Specific Distal Regulatory Sequence of Murine Sox17.Genes to cells : devoted to molecular & cellular mechanisms · 2025Article
- Generation of human induced pluripotent stem cell lines derived from patients of cystic biliary atresia.Human cell · 2024Article
- Sox17 and Other SoxF-Family Proteins Play Key Roles in the Hematopoiesis of Mouse Embryos.Cells · 2024Review
- Impact of gallbladder hypoplasia on hilar hepatic ducts in biliary atresia.Communications medicine · 2024Article
- Biliary atresia is associated with polygenic susceptibility in ciliogenesis and planar polarity effector genes.Journal of hepatology · 2023Article
- Biliatresone induces cholangiopathy in C57BL/6J neonates.Scientific reports · 2023Article
- Sox17 mediates adult arterial endothelial cell adaptation to hemodynamics.Biomaterials · 2023Article
- Development of extrahepatic bile ducts and mechanisms of tumorigenesis: Lessons from mouse models.Pathology international · 2022Review
- Differential regulation of alternate promoter regions iniScience · 2022Article
- Biliary Atresia Animal Models: Is the Needle in a Haystack?International journal of molecular sciences · 2022Review
- Biliary Atresia: A Complex Hepatobiliary Disease with Variable Gene Involvement, Diagnostic Procedures, and Prognosis.Diagnostics (Basel, Switzerland) · 2022Review
- A joint transcriptional regulatory network and protein activity inference analysis identifies clinically associated master regulators for biliary atresia.Frontiers in pediatrics · 2022Article
- Sry-related High Mobility Group Box 17 Functions as a Tumor Suppressor by Antagonizing the Wingless-related Integration Site Pathway.Journal of cancer prevention · 2020Review
- Whole exome sequencing analysis for mutations in isolated type III biliary atresia patients.Clinical and experimental hepatology · 2020Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
Congenital biliary atresia is an incurable disease of newborn infants, of unknown genetic causes, that results in congenital deformation of the gallbladder and biliary duct system. Here, we show that during mouse organogenesis, insufficient SOX17 expression in the gallbladder and bile duct epithelia results in congenital biliary atresia and subsequent acute 'embryonic hepatitis', leading to perinatal death in ~95% of the Sox17 heterozygote neonates in C57BL/6 (B6) background mice. During gallbladder and bile duct development, Sox17 was expressed at the distal edge of the gallbladder primordium. In the Sox17(+/-) B6 embryos, gallbladder epithelia were hypoplastic, and some were detached from the luminal wall, leading to bile duct stenosis or atresia. The shredding of the gallbladder epithelia is probably caused by cell-autonomous defects in proliferation and maintenance of the Sox17(+/-) gallbladder/bile duct epithelia. Our results suggest that Sox17 plays a dosage-dependent function in the morphogenesis and maturation of gallbladder and bile duct epithelia during the late-organogenic stages, highlighting a novel entry point to the understanding of the etiology and pathogenesis of human congenital biliary atresia.
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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.