ArticleGenome research2010
An integrative genomic analysis identifies Bhmt2 as a diet-dependent genetic factor protecting against acetaminophen-induced liver toxicity.
Article in Genome research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 46 citations in OpenAlex.
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- Preserving mitochondrial homeostasis protects against drug-induced liver injury via inducing OPTN (optineurin)-dependent Mitophagy.Autophagy · 2024Article
- Analysis of structural variation among inbred mouse strains.BMC genomics · 2023Article
- An automated multi-modal graph-based pipeline for mouse genetic discovery.Bioinformatics (Oxford, England) · 2022Article
- The Effect of Population Structure on Murine Genome-Wide Association Studies.Frontiers in genetics · 2021Article
- What Have We Learned (or Expect to) From Analysis of Murine Genetic Models Related to Substance Use Disorders?Frontiers in psychiatry · 2021Review
- Betaine-homocysteineFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Expression Levels of GABA-A Receptor Subunit Alpha 3,Biomolecules & therapeutics · 2017Article
- Long-Term Dietary Folate Deficiency Accelerates Progressive Hearing Loss on CBA/Ca Mice.Frontiers in aging neuroscience · 2016Article
- Predose and Postdose Blood Gene Expression Profiles Identify the Individuals Susceptible to Acetaminophen-Induced Liver Injury in Rats.PloS one · 2015Article
- Evolutionary Analyses and Natural Selection of Betaine-Homocysteine S-Methyltransferase (BHMT) and BHMT2 Genes.PloS one · 2015Article
- Identification of chemical modulators of the constitutive activated receptor (CAR) in a gene expression compendium.Nuclear receptor signaling · 2015Article
- Article
- Candidate gene polymorphisms in patients with acetaminophen-induced acute liver failure.Drug metabolism and disposition: the biological fate of chemicals · 2014Article
- New quantitative trait loci for carotid atherosclerosis identified in an intercross derived from apolipoprotein E-deficient mouse strains.Physiological genomics · 2013Article
- Fibroblast growth factor 21 is not required for the antidiabetic actions of the thiazoladinediones.Molecular metabolism · 2013Article
- A mouse diversity panel approach reveals the potential for clinical kidney injury due to DB289 not predicted by classical rodent models.Toxicological sciences : an official journal of the Society of Toxicology · 2012Article
- A better prognosis for genetic association studies in mice.Trends in genetics : TIG · 2012Article
- Evaluation of an in vitro toxicogenetic mouse model for hepatotoxicity.Toxicology and applied pharmacology · 2010Article
Corrections and comments
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Authors and funding
26 authors at 6 institutions in 2 countries.
Funding
Abstract
Acetaminophen-induced liver toxicity is the most frequent precipitating cause of acute liver failure and liver transplant, but contemporary medical practice has mainly focused on patient management after a liver injury has been induced. An integrative genetic, transcriptional, and two-dimensional NMR-based metabolomic analysis performed using multiple inbred mouse strains, along with knowledge-based filtering of these data, identified betaine-homocysteine methyltransferase 2 (Bhmt2) as a diet-dependent genetic factor that affected susceptibility to acetaminophen-induced liver toxicity in mice. Through an effect on methionine and glutathione biosynthesis, Bhmt2 could utilize its substrate (S-methylmethionine [SMM]) to confer protection against acetaminophen-induced injury in vivo. Since SMM is only synthesized in plants, Bhmt2 exerts its beneficial effect in a diet-dependent manner. Identification of Bhmt2 and the affected biosynthetic pathway demonstrates how a novel method of integrative genomic analysis in mice can provide a unique and clinically applicable approach to a major public health problem.
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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.