ArticleDevelopment (Cambridge, England)2015
Casz1 is required for cardiomyocyte G1-to-S phase progression during mammalian cardiac development.
Article in Development (Cambridge, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- CASZ1 regulates the maturation of outer hair cells and is required for hearing in mice.iScience · 2026Article
- Dilated and Noncompaction Cardiomyopathy in a Pediatric Patient With Maternal CASZ1 Variant.JACC. Case reports · 2026Article
- Deep learning the dynamic regulatory sequence code of cardiac organoid differentiation.bioRxiv : the preprint server for biology · 2025Article
- Sex-specific response to A1BG loss results in female dilated cardiomyopathy.Biology of sex differences · 2025Article
- Amniotic membrane, a novel bioscaffold in cardiac diseases: from mechanism to applications.Frontiers in bioengineering and biotechnology · 2024Review
- Role of the CASZ1 transcription factor in tissue development and disease.European journal of medical research · 2023Review
- The Tbx20-TLE interaction is essential for the maintenance of the second heart field.Development (Cambridge, England) · 2023Article
- Review
- Missense Mutation in Human CHD4 Causes Ventricular Noncompaction by Repressing ADAMTS1.Circulation research · 2023Article
- Identification of a Novel de Novo Variant in the CASZ1 Causing a Rare Type of Dilated Cardiomyopathy.International journal of molecular sciences · 2022Article
- Exome sequencing in multiplex families with left-sided cardiac defects has high yield for disease gene discovery.PLoS genetics · 2022Article
- CHD4 is recruited by GATA4 and NKX2-5 to repress noncardiac gene programs in the developing heart.Genes & development · 2022Article
- Cardiac proteomics reveals sex chromosome-dependent differences between males and females that arise prior to gonad formation.Developmental cell · 2021Article
- Targeting cardiomyocyte proliferation as a key approach of promoting heart repair after injury.Molecular biomedicine · 2021Review
- CASZ1b is a novel transcriptional corepressor of mineralocorticoid receptor.Hypertension research : official journal of the Japanese Society of Hypertension · 2021Article
- Epigenome-Wide Association Study for All-Cause Mortality in a Cardiovascular Cohort Identifies Differential Methylation in Castor Zinc Finger 1 (Journal of the American Heart Association · 2019Article
- Conservation and divergence of protein pathways in the vertebrate heart.PLoS biology · 2019Article
- A novel de novo CASZ1 heterozygous frameshift variant causes dilated cardiomyopathy and left ventricular noncompaction cardiomyopathy.Molecular genetics & genomic medicine · 2019Article
- Proteomic-based approaches to cardiac development and disease.Current opinion in chemical biology · 2019Review
- Zinc and Zinc Transporters: Novel Regulators of Ventricular Myocardial Development.Pediatric cardiology · 2018Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Organ growth occurs through the integration of external growth signals during the G1 phase of the cell cycle to initiate DNA replication. Although numerous growth factor signals have been shown to be required for the proliferation of cardiomyocytes, genetic studies have only identified a very limited number of transcription factors that act to regulate the entry of cardiomyocytes into S phase. Here, we report that the cardiac para-zinc-finger protein CASZ1 is expressed in murine cardiomyocytes. Genetic fate mapping with an inducible Casz1 allele demonstrates that CASZ1-expressing cells give rise to cardiomyocytes in the first and second heart fields. We show through the generation of a cardiac conditional null mutation that Casz1 is essential for the proliferation of cardiomyocytes in both heart fields and that loss of Casz1 leads to a decrease in cardiomyocyte cell number. We further report that the loss of Casz1 leads to a prolonged or arrested S phase, a decrease in DNA synthesis, an increase in phospho-RB and a concomitant decrease in the cardiac mitotic index. Taken together, these studies establish a role for CASZ1 in mammalian cardiomyocyte cell cycle progression in both the first and second heart fields.
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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.