ArticleProceedings of the National Academy of Sciences of the United States of America1998
The tumor suppressor SMAD4/DPC4 is essential for epiblast proliferation and mesoderm induction in mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.
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Who cites it
120 citing papers in PubMed, 360 citations in OpenAlex.
- The Role of Somatic Mutation in Hereditary Hemorrhagic Telangiectasia Pathogenesis.Journal of clinical medicine · 2025Review
- Smad4 is essential for epiblast scaling and morphogenesis after implantation, but nonessential before implantation.Development (Cambridge, England) · 2024Article
- Advances and Challenges in Targeting TGF-β Isoforms for Therapeutic Intervention of Cancer: A Mechanism-Based Perspective.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Article
- SMAD4: A critical regulator of cardiac neural crest cell fate and vascular smooth muscle development.Developmental dynamics : an official publication of the American Association of Anatomists · 2024Article
- Transcriptional network governing extraembryonic endoderm cell fate choice.Developmental biology · 2023Article
- Identifying novel regulators of placental development using time-series transcriptome data.Life science alliance · 2023Article
- Tumor models to assess immune response and tumor-microbiome interactions in colorectal cancer.Pharmacology & therapeutics · 2022Review
- Nhlrc2 is crucial during mouse gastrulation.Genesis (New York, N.Y. : 2000) · 2022Article
- Organ-Specific Endothelial Cell Differentiation and Impact of Microenvironmental Cues on Endothelial Heterogeneity.International journal of molecular sciences · 2022Review
- The versatility and paradox of BMP signaling in endothelial cell behaviors and blood vessel function.Cellular and molecular life sciences : CMLS · 2022Review
- Human Induced Pluripotent Stem Cell-Derived Vascular Cells: Recent Progress and Future Directions.Journal of cardiovascular development and disease · 2021Review
- Set1 Targets Genes with Essential Identity and Tumor-Suppressing Functions in Planarian Stem Cells.Genes · 2021Article
- Transforming growth factor beta signaling functions during mammalian kidney development.Pediatric nephrology (Berlin, Germany) · 2021Review
- Self-organized signaling in stem cell models of embryos.Stem cell reports · 2021Review
- Acromelic dysplasias: how rare musculoskeletal disorders reveal biological functions of extracellular matrix proteins.Annals of the New York Academy of Sciences · 2021Article
- BMP signalling is required for extra-embryonic ectoderm development during pre-to-post-implantation transition of the mouse embryo.Developmental biology · 2021Article
- Genetics and signaling mechanisms of orofacial clefts.Birth defects research · 2020Review
- Smad3 gene C-terminal phosphorylation site mutation aggravates CClJournal of cellular and molecular medicine · 2020Article
- Inhibition of plasminogen activator inhibitor-1 attenuates against intestinal fibrosis in mice.Intestinal research · 2020Article
60 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Members of the transforming growth factor (TGF)-beta superfamily have been shown to play a variety of important roles in embryogenesis, including dorsal and ventral mesoderm induction. The tumor suppressor SMAD4, also known as DPC4, is believed to be an essential factor that mediates TGF-beta signals. To explore functions of SMAD4 in development, we have mutated it by truncating its functional C-domain. We show that Smad4 is expressed ubiquitously during murine embryogenesis. Mice heterozygous for the Smad4(ex8/+) mutation are developmentally normal, whereas homozygotes die between embryonic day 6.5 (E6.5) and 8.5. All Smad4(ex8/ex8) mutants are developmentally delayed at E6 and show little or no elongation in the extraembryonic portion of late egg cylinder stage embryos. Consistent with this, cultured Smad4(ex8/ex8) blastocyst outgrowths suffer cellular proliferation defects and fail to undergo endoderm differentiation. Although a portion of mutant embryos at E8.5 show an increase in the embryonic ectoderm and endoderm, morphological and molecular analyses indicate that they do not form mesoderm. Altogether, these data demonstrate that SMAD4-mediated signals are required for epiblast proliferation, egg cylinder formation, and mesoderm induction.
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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.