ArticleMolecular and cellular biology2005
Smad1 and Smad8 function similarly in mammalian central nervous system development.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
The trial behind it
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
11 citing papers in PubMed, 24 citations in OpenAlex.
- BuMPing Into Neurogenesis: How the Canonical BMP Pathway Regulates Neural Stem Cell Divisions Throughout Space and Time.Frontiers in neuroscience · 2021Review
- Bu-M-P-ing Iron: How BMP Signaling Regulates Muscle Growth and Regeneration.Journal of developmental biology · 2020Review
- Tfap2a-dependent changes in mouse facial morphology result in clefting that can be ameliorated by a reduction in Fgf8 gene dosage.Disease models & mechanisms · 2015Article
- CHD7 interacts with BMP R-SMADs to epigenetically regulate cardiogenesis in mice.Human molecular genetics · 2014Article
- The multiple activities of BMPs during spinal cord development.Cellular and molecular life sciences : CMLS · 2013Review
- Co-ordinating Notch, BMP, and TGF-β signaling during heart valve development.Cellular and molecular life sciences : CMLS · 2013Review
- Defective pulmonary vascular remodeling in Smad8 mutant mice.Human molecular genetics · 2009Article
- Association study in the 5q31-32 linkage region for schizophrenia using pooled DNA genotyping.BMC psychiatry · 2008Article
- Inactivation of Smad5 in endothelial cells and smooth muscle cells demonstrates that Smad5 is required for cardiac homeostasis.The American journal of pathology · 2007Article
- The MH1 domain of Smad3 interacts with Pax6 and represses autoregulation of the Pax6 P1 promoter.Nucleic acids research · 2007Article
- Dose-dependent Smad1, Smad5 and Smad8 signaling in the early mouse embryo.Developmental biology · 2006Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Smads 1, 5, and 8 are the intracellular mediators for the bone morphogenetic proteins (BMPs), which play crucial roles during mammalian development. Previous research has shown that Smad1 is important in the formation of the allantois, while Smad5 has been shown to be critical in the process of angiogenesis. To further analyze the BMP-responsive Smads, we disrupted the murine Smad8 gene utilizing the Cre/loxP system. A Smad8 hypomorphic allele (Smad8(Deltaexon3)) was constructed that contains an in-frame deletion of exon 3, removing one-third of the MH2 domain and a small portion of the linker region. Xenopus injection assays indicated that this Smad8 deletion allele is still functional but has reduced ventralizing capability compared to the wild type. Although Smad8(Deltaexon3/Deltaexon3) embryos are phenotypically normal, homozygotes of another hypomorphic allele of Smad8 (Smad8(3loxP)) containing a neomycin cassette within intron 3, phenocopy an embryonic brain defect observed in roughly 22% of Smad1(+/)(-) embryos analyzed at embryonic day 11.5. These observations suggest that BMP-responsive Smads have critical functions in the development of the mammalian central nervous system.
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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.