ArticleThe Journal of biological chemistry2014
Essential role of the zinc finger transcription factor Casz1 for mammalian cardiac morphogenesis and development.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Identification of risk loci for primary aldosteronism in genome-wide association studies.Nature communications · 2022Pooled it
- Rare germline variants in canonical and candidate genes in apparently sporadic bilateral primary aldosteronism.Journal of the Endocrine Society · 2026Article
- Dilated and Noncompaction Cardiomyopathy in a Pediatric Patient With Maternal CASZ1 Variant.JACC. Case reports · 2026Article
- Dynamic proteome profiling of differentiating human embryonic stem cells towards cardiomyocytes.Scientific reports · 2025Article
- Deep learning the dynamic regulatory sequence code of cardiac organoid differentiation.bioRxiv : the preprint server for biology · 2025Article
- Radiation with reproductive isolation in the near-absence of phylogenetic signal.Science advances · 2025Article
- SCIG: Machine learning uncovers cell identity genes in single cells by genetic sequence codes.Nucleic acids research · 2025Article
- DNA-damage-associated protein co-expression network in cardiomyocytes informs on tolerance to genetic variation and disease.iScience · 2025Article
- SMYD1 modulates the proliferation of multipotent cardiac progenitor cells derived from human pluripotent stem cells during myocardial differentiation through GSK3β/β-catenin&ERK signaling.Stem cell research & therapy · 2024Article
- CASZ1 Is Essential for Skin Epidermal Terminal Differentiation.The Journal of investigative dermatology · 2024Article
- Role of the CASZ1 transcription factor in tissue development and disease.European journal of medical research · 2023Review
- Review
- Cooperative regulation of Zhx1 and hnRNPA1 drives the cardiac progenitor-specific transcriptional activation during cardiomyocyte differentiation.Cell death discovery · 2023Article
- Zinc finger transcription factor CASZ1b is involved in the DNA damage response in live cells.Biochemical and biophysical research communications · 2023Article
- Endothelial deletion of PTBP1 disrupts ventricular chamber development.Nature communications · 2023Article
- CASZ1 promotes migration, invasion, and metastasis of lung cancer cells by controlling expression of ITGAV.American journal of cancer research · 2023Article
- Actin cytoskeleton in angiogenesis.Biology open · 2022Review
- Identification of a Novel de Novo Variant in the CASZ1 Causing a Rare Type of Dilated Cardiomyopathy.International journal of molecular sciences · 2022Article
- Loss of CASZ1 tumor suppressor linked to oncogenic subversion of neuroblastoma core regulatory circuitry.Cell death & disease · 2022Article
- Detection of repeat expansions in large next generation DNA and RNA sequencing data without alignment.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
Chromosome 1p36 deletion syndrome is one of the most common terminal deletions observed in humans and is related to congenital heart disease (CHD). However, the 1p36 genes that contribute to heart disease have not been clearly delineated. Human CASZ1 gene localizes to 1p36 and encodes a zinc finger transcription factor. Casz1 is required for Xenopus heart ventral midline progenitor cell differentiation. Whether Casz1 plays a role during mammalian heart development is unknown. Our aim is to determine 1p36 gene CASZ1 function at regulating heart development in mammals. We generated a Casz1 knock-out mouse using Casz1-trapped embryonic stem cells. Casz1 deletion in mice resulted in abnormal heart development including hypoplasia of myocardium, ventricular septal defect, and disorganized morphology. Hypoplasia of myocardium was caused by decreased cardiomyocyte proliferation. Comparative genome-wide RNA transcriptome analysis of Casz1 depleted embryonic hearts identifies abnormal expression of genes that are critical for muscular system development and function, such as muscle contraction genes TNNI2, TNNT1, and CKM; contractile fiber gene ACTA1; and cardiac arrhythmia associated ion channel coding genes ABCC9 and CACNA1D. The transcriptional regulation of some of these genes by Casz1 was also found in cellular models. Our results showed that loss of Casz1 during mouse development led to heart defect including cardiac noncompaction and ventricular septal defect, which phenocopies 1p36 deletion syndrome related CHD. This suggests that CASZ1 is a novel 1p36 CHD gene and that the abnormal expression of cardiac morphogenesis and contraction genes induced by loss of Casz1 contributes to the heart defect.
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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.