ArticleDevelopmental biology2016
Neural crest requires Impdh2 for development of the enteric nervous system, great vessels, and craniofacial skeleton.
Article in Developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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
14 citing papers in PubMed, 24 citations in OpenAlex.
- IMPDH and GTP Metabolism in Cancer: Mechanisms, Regulation, and Translational Scope.Cancer science · 2025Review
- IMPDH2's Central Role in Cellular Growth and Diseases: A Potential Therapeutic Target.Cell proliferation · 2025Review
- Purine Metabolism and Dystonia: Perspectives of a Long-Promised Relationship.Annals of neurology · 2025Review
- Conditional deletion of IPJournal of gastroenterology · 2025Article
- Appendage regeneration requires IMPDH2 and creates a sensitized environment for enzyme filament formation.bioRxiv : the preprint server for biology · 2024Article
- BAP1 is required prenatally for differentiation and maintenance of postnatal murine enteric nervous system.The Journal of clinical investigation · 2024Article
- Rare variants in IMPDH2 cause autosomal dominant dystonia in Chinese population.Journal of neurology · 2023Article
- MicroRNA-1 affects the development of the neural crest and craniofacial skeleton via the mitochondrial apoptosis pathway.Experimental and therapeutic medicine · 2021Article
- scRNA-Seq Reveals New Enteric Nervous System Roles for GDNF, NRTN, and TBX3.Cellular and molecular gastroenterology and hepatology · 2021Article
- Monogenic variants in dystonia: an exome-wide sequencing study.The Lancet. Neurology · 2020Article
- GTP metabolic reprogramming by IMPDH2: unlocking cancer cells' fuelling mechanism.Journal of biochemistry · 2020Review
- Loss of Tbx3 in murine neural crest reduces enteric glia and causes cleft palate, but does not influence heart development or bowel transit.Developmental biology · 2018Article
- Muscularis macrophage development in the absence of an enteric nervous system.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Mouse models of Hirschsprung disease and other developmental disorders of the enteric nervous system: Old and new players.Developmental biology · 2016Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Mutations that impair the proliferation of enteric neural crest-derived cells (ENCDC) cause Hirschsprung disease, a potentially lethal birth defect where the enteric nervous system (ENS) is absent from distal bowel. Inosine 5' monophosphate dehydrogenase (IMPDH) activity is essential for de novo GMP synthesis, and chemical inhibition of IMPDH induces Hirschsprung disease-like pathology in mouse models by reducing ENCDC proliferation. Two IMPDH isoforms are ubiquitously expressed in the embryo, but only IMPDH2 is required for life. To further understand the role of IMPDH2 in ENS and neural crest development, we characterized a conditional Impdh2 mutant mouse. Deletion of Impdh2 in the early neural crest using the Wnt1-Cre transgene produced defects in multiple neural crest derivatives including highly penetrant intestinal aganglionosis, agenesis of the craniofacial skeleton, and cardiac outflow tract and great vessel malformations. Analysis using a Rosa26 reporter mouse suggested that some or all of the remaining ENS in Impdh2 conditional-knockout animals was derived from cells that escaped Wnt1-Cre mediated DNA recombination. These data suggest that IMPDH2 mediated guanine nucleotide synthesis is essential for normal development of the ENS and other neural crest derivatives.
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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.