ArticleJournal of molecular and cellular cardiology2010
Partial rescue of the Tbx1 mutant heart phenotype by Fgf8: genetic evidence of impaired tissue response to Fgf8.
Article in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 26 citations in OpenAlex.
- In-silico identification of deleterious non-synonymous SNPs of TBX1 gene: Functional and structural impact towards 22q11.2DS.PloS one · 2024Article
- Human stem cell-derived thymic epithelial cells enhance human T-cell development in a xenogeneic thymus.The Journal of allergy and clinical immunology · 2022Article
- Understanding Heart Field Progenitor Cells for Modeling Congenital Heart Diseases.Current cardiology reports · 2021Review
- Pharmacological Rescue of the Brain Cortex Phenotype ofFrontiers in molecular neuroscience · 2021Article
- A novel source of arterial valve cells linked to bicuspid aortic valve without raphe in mice.eLife · 2018Article
- Three TF Co-expression Modules Regulate Pressure-Overload Cardiac Hypertrophy in Male Mice.Scientific reports · 2017Article
- Vitamin B12 ameliorates the phenotype of a mouse model of DiGeorge syndrome.Human molecular genetics · 2016Article
- Loss of Wnt5a disrupts second heart field cell deployment and may contribute to OFT malformations in DiGeorge syndrome.Human molecular genetics · 2015Article
- Endoderm-specific deletion of Tbx1 reveals an FGF-independent role for Tbx1 in pharyngeal apparatus morphogenesis.Developmental dynamics : an official publication of the American Association of Anatomists · 2014Article
- Tbx1 is required for second heart field proliferation in zebrafish.Developmental dynamics : an official publication of the American Association of Anatomists · 2013Article
- The neural crest in cardiac congenital anomalies.Differentiation; research in biological diversity · 2012Review
- Signaling in cell differentiation and morphogenesis.Cold Spring Harbor perspectives in biology · 2012Review
- Identification of a Tbx1/Tbx2/Tbx3 genetic pathway governing pharyngeal and arterial pole morphogenesis.Human molecular genetics · 2012Article
- A Tbx1-Six1/Eya1-Fgf8 genetic pathway controls mammalian cardiovascular and craniofacial morphogenesis.The Journal of clinical investigation · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Tbx1 is the candidate gene of DiGeorge syndrome and is required in humans and mice for the development of the cardiac outflow tract (OFT) and aortic arch arteries. Loss of function mutants present with reduced cell proliferation and premature differentiation of cardiac progenitor cells of the second heart field (SHF). Tbx1 regulates Fgf8 expression hence the hypothesis that the proliferation impairment may contribute to the heart phenotype of mutants. Here we show that forced Fgf8 expression modifies and partially rescues the OFT septation defects of Tbx1 mutants but only if there is some residual expression of Tbx1. This genetic experiment suggests that Tbx1, directly or indirectly, affects tissue response to Fgf8. Indeed, Tbx1(-/-) mouse embryonic fibroblasts were unable to respond to Fgf8 added to the culture media and showed defective response of Erk1/2 and Rsk1. Our data suggest a coordinated pathway modulating Fgf8 ligand expression and tissue response to it in the SHF.
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.