ArticleHepatology (Baltimore, Md.)2008
A facile method for somatic, lifelong manipulation of multiple genes in the mouse liver.
Article in Hepatology (Baltimore, Md.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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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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
40 citing papers in PubMed, 64 citations in OpenAlex.
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- DNA Deamination Is Required for Human APOBEC3A-Driven Hepatocellular Carcinoma In Vivo.International journal of molecular sciences · 2023Article
- Cellular origins of regenerating liver and hepatocellular carcinoma.JHEP reports : innovation in hepatology · 2022Review
- The Effects and Underlying Mechanisms of Hepatitis B Virus X Gene Mutants on the Development of Hepatocellular Carcinoma.Frontiers in oncology · 2022Article
- ZBTB20 regulates WNT/CTNNB1 signalling pathway by suppressing PPARG during hepatocellular carcinoma tumourigenesis.JHEP reports : innovation in hepatology · 2021Article
- A Three-Dimensional Imaging Method for the Quantification and Localization of Dynamic Cell Tracking Posttransplantation.Frontiers in cell and developmental biology · 2021Article
- APOBEC3A catalyzes mutation and drives carcinogenesis in vivo.The Journal of experimental medicine · 2020Article
- Cell-Autonomous Autophagy Protects Against Chronic Intermittent Hypoxia Induced Sensory Nerves and Endothelial Dysfunction of the Soft Palate.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Oncogenic driver genes and tumor microenvironment determine the type of liver cancer.Cell death & disease · 2020Review
- A High-Content Screen Identifies MicroRNAs That Regulate Liver Repopulation After Injury in Mice.Gastroenterology · 2020Article
- The Dynamic Chromatin Architecture of the Regenerating Liver.Cellular and molecular gastroenterology and hepatology · 2020Article
- Cell Type-specific Gene Expression Profiling in the Mouse Liver.Journal of visualized experiments : JoVE · 2019Article
- HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism.Molecular cancer research : MCR · 2019Article
- Liver Cancer Gene Discovery Using Gene Targeting, Sleeping Beauty, and CRISPR/Cas9.Seminars in liver disease · 2019Review
- Combinatorial genetics in liver repopulation and carcinogenesis with a in vivo CRISPR activation platform.Hepatology (Baltimore, Md.) · 2018Article
- TRAP-seq identifies cystine/glutamate antiporter as a driver of recovery from liver injury.The Journal of clinical investigation · 2018Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
unlabelledCurrent techniques for the alteration of gene expression in the liver have a number of limitations, including the lack of stable somatic gene transfer and the technical challenges of germline transgenesis. Rapid and stable genetic engineering of the liver would allow systematic, in vivo testing of contributions by many genes to disease. After fumaryl acetoacetate hydrolase (Fah) gene transfer to hepatocytes, selective repopulation of the liver occurs in FAH-deficient mice. This genetic correction is readily mediated with transposons. Using this approach, we show that genes with biological utility can be linked to a selectable Fah transposon cassette. First, net conversion of Fah(-/-) liver tissue to transgenic tissue, and its outgrowth, was monitored by bioluminescence in vivo from a luciferase gene linked to the FAH gene. Second, coexpressed short hairpin RNAs (shRNAs) stably reduced target gene expression, indicating the potential for loss-of-function assays. Third, a mutant allele of human alpha1-antitrypsin (hAAT) was linked to Fah and resulted in protein inclusions within hepatocytes, which are the histopathological hallmark of hAAT deficiency disorder. Finally, oncogenes linked to Fah resulted in transformation of transduced hepatocytes.
conclusionCoexpression with FAH is an effective technique for lifelong expression of transgenes in adult hepatocytes with applicability to a wide variety of genetic studies in the liver.
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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.