@article{Liu01012010,
author = {Liu, Hong-Hsing and Lu, Peng and Guo, Yingying and Farrell, Erin and Zhang, Xun and Zheng, Ming and Bosano, Betty and Zhang, Zhaomei and Allard, John and Liao, Guochun and Fu, Siyu and Chen, Jinzhi and Dolim, Kimberly and Kuroda, Ayako and Usuka, Jonathan and Cheng, Janet and Tao, William and Welch, Kevin and Liu, Yanzhou and Pease, Joseph and de Keczer, Steve A. and Masjedizadeh, Mohammad and Hu, Jing-Shan and Weller, Paul and Garrow, Tim and Peltz, Gary}, 
title = {An integrative genomic analysis identifies Bhmt2 as a diet-dependent genetic factor protecting against acetaminophen-induced liver toxicity},
volume = {20}, 
number = {1}, 
pages = {28-35}, 
year = {2010}, 
doi = {10.1101/gr.097212.109}, 
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.}, 
URL = {http://genome.cshlp.org/content/20/1/28.abstract}, 
eprint = {http://genome.cshlp.org/content/20/1/28.full.pdf+html}, 
journal = {Genome Research} 
}