ArticleProceedings of the National Academy of Sciences of the United States of America2015
Maternal and zygotic Zfp57 modulate NOTCH signaling in cardiac development.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Allele-specific CRISPR perturbation of the imprinted Dlk1-Dio3 domain reveals regulation of BMP-NOTCH-VEGF signaling in embryonic organogenesis.Cell death and differentiation · 2026Article
- Ets1-regulated endothelial-secreted factors promote compact myocardial growth and contribute to the pathogenesis of ventricular non-compaction.Cardiovascular research · 2026Article
- ZFP57 is a regulator of postnatal growth and life-long health.Nature communications · 2026Article
- LncRNAs in theInternational journal of molecular sciences · 2024Article
- Pericardial delta like non-canonical NOTCH ligand 1 (Dlk1) augments fibrosis in the heart through epithelial to mesenchymal transition.Clinical and translational medicine · 2024Article
- Charting the Path: Navigating Embryonic Development to Potentially Safeguard against Congenital Heart Defects.Journal of personalized medicine · 2023Review
- CpG site hypomethylation at ETS1‑binding region regulates DLK1 expression in Chinese patients with Tetralogy of Fallot.Molecular medicine reports · 2022Article
- Maternal effect genes: Update and review of evidence for a link with birth defects.HGG advances · 2022Review
- Article
- Developmental toxicant exposures and sex-specific effects on epigenetic programming and cardiovascular health across generations.Environmental epigenetics · 2022Review
- ZFP57 dictates allelic expression switch of target imprinted genes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- NOTCH Receptors and DLK Proteins Enhance Brown Adipogenesis in Mesenchymal C3H10T1/2 Cells.Cells · 2020Article
- Dlk1-Mediated Temporal Regulation of Notch Signaling Is Required for Differentiation of Alveolar Type II to Type I Cells during Repair.Cell reports · 2019Article
- DNA Methylation Readers and Cancer: Mechanistic and Therapeutic Applications.Frontiers in oncology · 2019Review
- Gene expression profiles of glomerular endothelial cells support their role in the glomerulopathy of diabetic mice.Kidney international · 2018Article
- ZFP57 maintains the parent-of-origin-specific expression of the imprinted genes and differentially affects non-imprinted targets in mouse embryonic stem cells.Nucleic acids research · 2016Article
- Cardiac Embryology and Molecular Mechanisms of Congenital Heart Disease: A Primer for Anesthesiologists.Anesthesia and analgesia · 2016Review
- Mechanisms and Disease Associations of Haplotype-Dependent Allele-Specific DNA Methylation.American journal of human genetics · 2016Article
- Zfp57 mutant ES cell lines directly derived from blastocysts.Stem cell research · 2016Article
- Genomic imprinting defect in Zfp57 mutant iPS cell lines.Stem cell research · 2016Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
Zfp57 is a maternal-zygotic effect gene that maintains genomic imprinting. Here we report that Zfp57 mutants exhibited a variety of cardiac defects including atrial septal defect (ASD), ventricular septal defect (VSD), thin myocardium, and reduced trabeculation. Zfp57 maternal-zygotic mutant embryos displayed more severe phenotypes with higher penetrance than the zygotic ones. Cardiac progenitor cells exhibited proliferation and differentiation defects in Zfp57 mutants. ZFP57 is a master regulator of genomic imprinting, so the DNA methylation imprint was lost in embryonic heart without ZFP57. Interestingly, the presence of imprinted DLK1, a target of ZFP57, correlated with NOTCH1 activation in cardiac cells. These results suggest that ZFP57 may modulate NOTCH signaling during cardiac development. Indeed, loss of ZFP57 caused loss of NOTCH1 activation in embryonic heart with more severe loss observed in the maternal-zygotic mutant. Maternal and zygotic functions of Zfp57 appear to play redundant roles in NOTCH1 activation and cardiomyocyte differentiation. This serves as an example of a maternal effect that can influence mammalian organ development. It also links genomic imprinting to NOTCH signaling and particular developmental functions.
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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.