ArticleGenes & development2004
Hedgehog signaling in the neural crest cells regulates the patterning and growth of facial primordia.
Article in Genes & development, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 359 papers, 1 of them a synthesis that pooled it.
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Who cites it
359 citing papers in PubMed, 1 synthesis or guideline pooled it, 633 citations in OpenAlex.
- Conservation of Epithelial-to-Mesenchymal Transition Process in Neural Crest Cells and Metastatic Cancer.Cells, tissues, organs · 2021Pooled it
- Local delivery of interferon restores antigen presentation and sensitizes medulloblastoma to T cell killing.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Sharp cell type boundaries emerge from coordinated morphogen signaling.Genes & development · 2026Article
- Identification of novel genes regulating the development of the palate.Developmental dynamics : an official publication of the American Association of Anatomists · 2026Article
- Effects of Smoothened Agonist Exposure on Murine Craniofacial Development.International dental journal · 2026Article
- A cross-tissue physicochemical causal chain underlying vertebrate mandibular morphogenesis.Science advances · 2026Article
- Computational Mapping of Hedgehog Pathway Kinase Module Predicts Node-Specific Craniofacial Phenotypes.Genes · 2026Article
- A transcription regulator atlas identifies TOX3 as an Atoh1 coactivator in cerebellar development and tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Gli2 and Gli3 synergistically mediate HH-TGF-β crosstalk in mesenchymal progenitor cells to orchestrate tooth root morphogenesis.International journal of oral science · 2026Article
- Plagl1 regulates the retinal progenitor cell to Müller glial cell transition.PLoS genetics · 2026Article
- Stc1-expressing myofibroblasts are a developmentally distinct lineage cleared through apoptosis in the neonatal lung.Cell reports · 2026Article
- Non-cell-autonomous tumor promotion in DICER1 cancer predisposition.Developmental cell · 2026Article
- Loss of SPECC1L in cranial neural crest cells results in increased hedgehog signaling and frontonasal dysplasia.Frontiers in physiology · 2026Article
- A dual role for GLI3 signaling in neural crest development.Development (Cambridge, England) · 2026Article
- Article
- Loss of SPECC1L in cranial neural crest cells results in increased hedgehog signaling and frontonasal dysplasia.bioRxiv : the preprint server for biology · 2025Article
- Transdifferentiation of endothelial progenitor cells into rhabdomyosarcoma defined by hedgehog signaling competence.Cell reports · 2025Article
- Alternative spliceosomal protein Eftud2 mediated Kif3a exon skipping promotes SHH-subgroup medulloblastoma progression.Cell death and differentiation · 2025Article
- Dual Bmp-negative feedback loops modulate function of both AER and ZPA to buffer and constrain postaxial digit number.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cranial base synostosis in mice caused by upregulation of Wnt following partial inhibition of Shh.BMC biology · 2025Article
299 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Facial abnormalities in human SHH mutants have implicated the Hedgehog (Hh) pathway in craniofacial development, but early defects in mouse Shh mutants have precluded the experimental analysis of this phenotype. Here, we removed Hh-responsiveness specifically in neural crest cells (NCCs), the multipotent cell type that gives rise to much of the skeleton and connective tissue of the head. In these mutants, many of the NCC-derived skeletal and nonskeletal components are missing, but the NCC-derived neuronal cell types are unaffected. Although the initial formation of branchial arches (BAs) is normal, expression of several Fox genes, specific targets of Hh signaling in cranial NCCs, is lost in the mutant. The spatially restricted expression of Fox genes suggests that they may play an important role in BA patterning. Removing Hh signaling in NCCs also leads to increased apoptosis and decreased cell proliferation in the BAs, which results in facial truncation that is evident by embryonic day 11.5 (E11.5). Together, our results demonstrate that Hh signaling in NCCs is essential for normal patterning and growth of the face. Further, our analysis of Shh-Fox gene regulatory interactions leads us to propose that Fox genes mediate the action of Shh in facial development.
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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.