ArticleDisease models & mechanisms2013
Functional validation of GWAS gene candidates for abnormal liver function during zebrafish liver development.
Article in Disease models & mechanisms, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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
21 citing papers in PubMed, 32 citations in OpenAlex.
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- Identification of Novel Vascular Genes Downstream of Islet2 and Nr2f1b Transcription Factors.Biomedicines · 2022Article
- Identification and functional validation of HLA-C as a potential gene involved in colorectal cancer in the Korean population.BMC genomics · 2022Article
- GCH1 Deficiency Activates Brain Innate Immune Response and Impairs Tyrosine Hydroxylase Homeostasis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Validation of Candidate Sleep Disorder Risk Genes Using Zebrafish.Frontiers in molecular neuroscience · 2022Review
- Generation of a Transgenic Zebrafish Line for In Vivo Assessment of Hepatic Apoptosis.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Roots and stems ofPharmaceutical biology · 2020Article
- MiRNAs and mRNAs Analysis during Abdominal Preadipocyte Differentiation in Chickens.Animals : an open access journal from MDPI · 2020Article
- Genetic deletion of gpr27 alters acylcarnitine metabolism, insulin sensitivity, and glucose homeostasis in zebrafish.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Using zebrafish to study skeletal genomics.Bone · 2019Review
- Toxicity Evaluation and Biomarker Selection with Validated Reference Gene in Embryonic Zebrafish Exposed to Mitoxantrone.International journal of molecular sciences · 2018Article
- Inorganic arsenic causes fatty liver and interacts with ethanol to cause alcoholic liver disease in zebrafish.Disease models & mechanisms · 2018Article
- Combining Zebrafish and CRISPR/Cas9: Toward a More Efficient Drug Discovery Pipeline.Frontiers in pharmacology · 2018Review
- Using zebrafish to model liver diseases-Where do we stand?Current pathobiology reports · 2017Article
- Fine-tune regulation of carboxypeptidase N1 controls vascular patterning during zebrafish development.Scientific reports · 2017Article
- ZeGlobalTox: An Innovative Approach to Address Organ Drug Toxicity Using Zebrafish.International journal of molecular sciences · 2017Article
- Function-driven discovery of disease genes in zebrafish using an integrated genomics big data resource.Nucleic acids research · 2016Article
- The lure of zebrafish in liver research: regulation of hepatic growth in development and regeneration.Current opinion in genetics & development · 2015Review
- Repairing quite swimmingly: advances in regenerative medicine using zebrafish.Disease models & mechanisms · 2014Review
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
Genome-wide association studies (GWAS) have revealed numerous associations between many phenotypes and gene candidates. Frequently, however, further elucidation of gene function has not been achieved. A recent GWAS identified 69 candidate genes associated with elevated liver enzyme concentrations, which are clinical markers of liver disease. To investigate the role of these genes in liver homeostasis, we narrowed down this list to 12 genes based on zebrafish orthology, zebrafish liver expression and disease correlation. To assess the function of gene candidates during liver development, we assayed hepatic progenitors at 48 hours post fertilization (hpf) and hepatocytes at 72 hpf using in situ hybridization following morpholino knockdown in zebrafish embryos. Knockdown of three genes (pnpla3, pklr and mapk10) decreased expression of hepatic progenitor cells, whereas knockdown of eight genes (pnpla3, cpn1, trib1, fads2, slc2a2, pklr, mapk10 and samm50) decreased cell-specific hepatocyte expression. We then induced liver injury in zebrafish embryos using acetaminophen exposure and observed changes in liver toxicity incidence in morphants. Prioritization of GWAS candidates and morpholino knockdown expedites the study of newly identified genes impacting liver development and represents a feasible method for initial assessment of candidate genes to instruct further mechanistic analyses. Our analysis can be extended to GWAS for additional disease-associated phenotypes.
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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.