ArticleDevelopment (Cambridge, England)2016
Six3 dosage mediates the pathogenesis of holoprosencephaly.
Article in Development (Cambridge, England), 2016. 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- SIX3 as a Regulator of Development and Disease.Journal of developmental biology · 2026Review
- Genetic and environmental factors contributing to anophthalmia and microphthalmia: Current understanding and future directions.World journal of clinical pediatrics · 2025Review
- Sine oculis homeobox homolog family function in gastrointestinal cancer: Progression and comprehensive analysis.World journal of clinical oncology · 2025Review
- Chd5 Regulates the Transcription Factor Six3 to Promote Neuronal Differentiation.Stem cells (Dayton, Ohio) · 2023Article
- Heterozygous variants in SIX3 and POU1F1 cause pituitary hormone deficiency in mouse and man.Human molecular genetics · 2023Article
- Homeobox Gene Six3 is Required for the Differentiation of D2-Type Medium Spiny Neurons.Neuroscience bulletin · 2021Article
- NewMolecular syndromology · 2021Article
- The SIX Family of Transcription Factors: Common Themes Integrating Developmental and Cancer Biology.Frontiers in cell and developmental biology · 2021Review
- Article
- The Homeodomain Transcription Factors Vax1 and Six6 Are Required for SCN Development and Function.Molecular neurobiology · 2020Article
- Developmental Genes and Malformations in the Hypothalamus.Frontiers in neuroanatomy · 2020Review
- SHH signaling mediated by a prechordal and brain enhancer controls forebrain organization.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Modeling the complex etiology of holoprosencephaly in mice.American journal of medical genetics. Part C, Seminars in medical genetics · 2018Review
- Article
- BOC is a modifier gene in holoprosencephaly.Human mutation · 2017Article
- SIX3, a tumor suppressor, inhibits astrocytoma tumorigenesis by transcriptional repression of AURKA/B.Journal of hematology & oncology · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Holoprosencephaly (HPE) is defined as the incomplete separation of the two cerebral hemispheres. The pathology of HPE is variable and, based on the severity of the defect, HPE is divided into alobar, semilobar, and lobar. Using a novel hypomorphic Six3 allele, we demonstrate in mice that variability in Six3 dosage results in different HPE phenotypes. Furthermore, we show that whereas the semilobar phenotype results from severe downregulation of Shh expression in the rostral diencephalon ventral midline, the alobar phenotype is caused by downregulation of Foxg1 expression in the anterior neural ectoderm. Consistent with these results, in vivo activation of the Shh signaling pathway rescued the semilobar phenotype but not the alobar phenotype. Our findings show that variations in Six3 dosage result in different forms of HPE.
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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.