ArticleGenesis (New York, N.Y. : 2000)2012
Generation of conditional alleles for Foxc1 and Foxc2 in mice.
Article in Genesis (New York, N.Y. : 2000), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- Pleiotropy in FOXC1-attributable phenotypes involves altered ciliation and cilia-dependent signaling.Scientific reports · 2024Article
- FOXC1 and FOXC2 regulate growth plate chondrocyte maturation towards hypertrophy in the embryonic mouse limb skeleton.Development (Cambridge, England) · 2024Article
- Identification of quiescent FOXC2eLife · 2023Article
- Endothelial FOXC1 and FOXC2 promote intestinal regeneration after ischemia-reperfusion injury.EMBO reports · 2023Article
- The genetics of glaucoma: Disease associations, personalised risk assessment and therapeutic opportunities-A review.Clinical & experimental ophthalmology · 2022Review
- Conditional inactivation of Foxc1 and Foxc2 in neural crest cells leads to cardiac abnormalities.Genesis (New York, N.Y. : 2000) · 2020Article
- Article
- Hemodynamic regulation of perivalvular endothelial gene expression prevents deep venous thrombosis.The Journal of clinical investigation · 2019Article
- Foxc2 is required for proper cardiac neural crest cell migration, outflow tract septation, and ventricle expansion.Developmental dynamics : an official publication of the American Association of Anatomists · 2018Article
- Human venous valve disease caused by mutations in FOXC2 and GJC2.The Journal of experimental medicine · 2017Article
- Foxc1 and Foxc2 in the Neural Crest Are Required for Ocular Anterior Segment Development.Investigative ophthalmology & visual science · 2017Article
- Foxc1 Ablated Mice Are Anhidrotic and Recapitulate Features of Human Miliaria Sweat Retention Disorder.The Journal of investigative dermatology · 2017Article
- Cerebrovascular defects in Foxc1 mutants correlate with aberrant WNT and VEGF-A pathways downstream of retinoic acid from the meninges.Developmental biology · 2016Article
- Foxc1 and Foxc2 deletion causes abnormal lymphangiogenesis and correlates with ERK hyperactivation.The Journal of clinical investigation · 2016Article
- FOXC1 maintains the hair follicle stem cell niche and governs stem cell quiescence to preserve long-term tissue-regenerating potential.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Endothelial cell specification in the somite is compromised in Pax3-positive progenitors of Foxc1/2 conditional mutants, with loss of forelimb myogenesis.Development (Cambridge, England) · 2016Article
- Conditional knockout of Foxc2 gene in kidney: efficient generation of conditional alleles of single-exon gene by double-selection system.Mammalian genome : official journal of the International Mammalian Genome Society · 2016Article
- Article
- Foxc1 is required by pericytes during fetal brain angiogenesis.Biology open · 2013Article
- FOXC1 is enriched in the mammary luminal progenitor population, but is not necessary for mouse mammary ductal morphogenesis.Biology of reproduction · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
The Forkhead box transcription factors, Foxc1 and Foxc2, are crucial for development of the eye, cardiovascular network, and other physiological systems, but their cell-type specific and postdevelopmental functions are unknown, in part because conventional (i.e., whole-organism) homozygous-null mutations of either factor result in perinatal death. Here, we describe the generation of mice with conditional-null Foxc1(flox) and Foxc2(flox) mutations that are induced via Cre-mediated recombination. Mice homozygous for the unrecombined alleles are viable and fertile, indicating that the conditional alleles retain their wild-type function. The embryos of Foxc1(flox) or Foxc2(flox) mice crossed with Cre-deleter mice that are homozygous for the recombined allele (i.e., Foxc1(Δ/Δ) or Foxc2(Δ/Δ) embryos) lack expression of the corresponding gene and show the same developmental defects observed in conventional homozygous mutant embryos. We expect these conditional mutations to enable characterization of the cell-type specific functions of Foxc1 and Foxc2 in development, disease, and adult animals.
Indexed as
Identifiers
What OpenQuestion holds
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.