ArticleDevelopment (Cambridge, England)2006
TBX5 is required for embryonic cardiac cell cycle progression.
Article in Development (Cambridge, England), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Pooled it
- Use of Frogs as a Model to Study the Etiology of HLHS.Journal of cardiovascular development and disease · 2023Article
- Swimming exercise with L-arginine coated nanoparticles supplementation upregulated HAND2 and TBX5 expression in the cardiomyocytes of aging male rats.Biogerontology · 2022Article
- Identification of a novel TBX5 c.755 + 1 G > A variant and related pathogenesis in a family with Holt-Oram syndrome.American journal of medical genetics. Part A · 2022Article
- Preclinical evidence for the therapeutic value of TBX5 normalization in arrhythmia control.Cardiovascular research · 2021Article
- miR-182-5p is an evolutionarily conserved Tbx5 effector that impacts cardiac development and electrical activity in zebrafish.Cellular and molecular life sciences : CMLS · 2020Article
- Review
- Pectoral Fin Anomalies inJournal of developmental biology · 2019Article
- Evolutionarily conservedProceedings of the National Academy of Sciences of the United States of America · 2018Article
- An interspecies heart-to-heart: UsingCurrent pathobiology reports · 2017Article
- TBX5: A Key Regulator of Heart Development.Current topics in developmental biology · 2017Review
- A Matter of the Heart: The African Clawed Frog Xenopus as a Model for Studying Vertebrate Cardiogenesis and Congenital Heart Defects.Journal of cardiovascular development and disease · 2016Review
- The Cardiac TBX5 Interactome Reveals a Chromatin Remodeling Network Essential for Cardiac Septation.Developmental cell · 2016Article
- Discovering miRNA Regulatory Networks in Holt-Oram Syndrome Using a Zebrafish Model.Frontiers in bioengineering and biotechnology · 2016Article
- Disruption of myocardial Gata4 and Tbx5 results in defects in cardiomyocyte proliferation and atrioventricular septation.Human molecular genetics · 2014Article
- Foxf genes integrate tbx5 and hedgehog pathways in the second heart field for cardiac septation.PLoS genetics · 2014Article
- Congenital heart disease protein 5 associates with CASZ1 to maintain myocardial tissue integrity.Development (Cambridge, England) · 2014Article
- Differential regulation of CASZ1 protein expression during cardiac and skeletal muscle development.Developmental dynamics : an official publication of the American Association of Anatomists · 2014Article
- A Gro/TLE-NuRD corepressor complex facilitates Tbx20-dependent transcriptional repression.Journal of proteome research · 2013Article
- A genetic assay of three patients in the same family with Holt-Oram syndrome; a case report.Reports of biochemistry & molecular biology · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Despite the critical importance of TBX5 in normal development and disease, relatively little is known about the mechanisms by which TBX5 functions in the embryonic heart. Our present studies demonstrate that TBX5 is necessary to control the length of the embryonic cardiac cell cycle, with depletion of TBX5 leading to cardiac cell cycle arrest in late G(1)- or early S-phase. Blocking cell cycle progression by TBX5 depletion leads to a decrease in cardiac cell number, an alteration in the timing of the cardiac differentiation program, defects in cardiac sarcomere formation, and ultimately, to cardiac programmed cell death. In these studies we have also established that terminally differentiated cardiomyocytes retain the capacity to undergo cell division. We further show that TBX5 is sufficient to determine the length of the embryonic cardiac cell cycle and the timing of the cardiac differentiation program. Thus, these studies establish a role for TBX5 in regulating the progression of the cardiac cell cycle.
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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.