ReviewSeminars in cell & developmental biology2016
Xenopus as a model organism for birth defects-Congenital heart disease and heterotaxy.
Review in Seminars in cell & developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed.
- Functional genomics iniScience · 2026Article
- Patient-informed CRISPR screen identifies FLNB as a congenital heart disease and ciliopathy gene.HGG advances · 2026Article
- Patient-informed CRISPR Screen Identifies FLNB as a Novel Congenital Heart Disease and Ciliopathy Gene.bioRxiv : the preprint server for biology · 2025Article
- Integrative Functional Genomics Identifies ARHGAP10 in the 4q31.2 Locus as a Novel Congenital Heart Disease and Ciliopathy Gene.bioRxiv : the preprint server for biology · 2025Article
- Ciliary biology intersects autism and congenital heart disease.Development (Cambridge, England) · 2025Article
- Efficient Techniques for Comprehensive Sampling of Accessible Tissues in Adult Xenopus.Journal of visualized experiments : JoVE · 2025Article
- CC2D1A causes ciliopathy, intellectual disability, heterotaxy, renal dysplasia, and abnormal CSF flow.Life science alliance · 2024Article
- Fbrsl1 is required for heart development in Xenopus laevis and de novo variants in FBRSL1 can cause human heart defects.Disease models & mechanisms · 2024Article
- Screening and regulatory mechanism exploration of M1 macrophage polarization and efferocytosis-related biomarkers in coronary heart disease.Frontiers in cardiovascular medicine · 2024Article
- Article
- Tissue disaggregation and isolation of specific cell types from transgenic Xenopus appendages for transcriptional analysis by FACS.Developmental dynamics : an official publication of the American Association of Anatomists · 2021Article
- Article
- Article
- Aquatic models of human ciliary diseases.Genesis (New York, N.Y. : 2000) · 2021Review
- Xenopus leads the way: Frogs as a pioneering model to understand the human brain.Genesis (New York, N.Y. : 2000) · 2021Review
- Mass spectrometry based proteomics for developmental neurobiology in the amphibian Xenopus laevis.Current topics in developmental biology · 2021Review
- Validating the Paradigm That Biomechanical Forces Regulate Embryonic Cardiovascular Morphogenesis and Are Fundamental in the Etiology of Congenital Heart Disease.Journal of cardiovascular development and disease · 2020Review
- Review
- Toward Decoding Bioelectric Events in Xenopus Embryogenesis: New Methodology for Tracking Interplay Between Calcium and Resting Potentials In Vivo.Journal of molecular biology · 2020Article
- An in vivo brain-bacteria interface: the developing brain as a key regulator of innate immunity.NPJ Regenerative medicine · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Congenital heart disease is the leading cause of birth defects, affecting 9 out of 1000 newborns each year. A particularly severe form of congenital heart disease is heterotaxy, a disorder of left-right development. Despite aggressive surgical management, patients with heterotaxy have poor survival rates and severe morbidity due to their complex congenital heart disease. Recent genetic analysis of affected patients has found novel candidate genes for heterotaxy although their underlying mechanisms remain unknown. In this review, we discuss the importance and challenges of birth defects research including high locus heterogeneity and few second alleles that make defining disease causality difficult. A powerful strategy moving forward is to analyze these candidate genes in a high-throughput human disease model. Xenopus is ideal for these studies. We present multiple examples demonstrating the power of Xenopus in discovering new biology from the analysis of candidate heterotaxy genes such as GALNT11, NEK2 and BCOR. These genes have diverse roles in embryos and have led to a greater understanding of complex signaling pathways and basic developmental biology. It is our hope that the mechanistic analysis of these candidate genes in Xenopus enabled by next generation sequencing of patients will provide clinicians with a greater understanding of patient pathophysiology allowing more precise and personalized medicine, to help patients more effectively in the future.
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.