The primary function of Omics Core is to provide members of the ULARC with the expertise, resources and facilities needed for metabolomic, proteomic and bioinformatic analyses of biological samples collected to study liver injury, nutrition, gut:liver interactions, and liver:environment/toxicant/drug interactions. OMICS Core personnel will assist with the design of sample collection protocols, will drive the development and the execution of novel and robust chromatographic methods for sample separation and mass spectrometric methods for the analysis of proteins, peptides, and metabolites with a goal of providing a greater understanding of the evolution of molecular mechanisms that correlate with or participate in liver dysfunction. The core will ensure uniformity and standardization in sample preparation, method development, instrument performance, data collection, data reporting and data sharing. The Core endeavors to contribute to the overall success and utility of the ULARC and to enhance the infrastructure and the technical and academic capabilities of the institution as a whole. In addition to its function as a service core, we will also promote the education and training of the ULARC members with regards to state-of?the-art Omics and Bioinformatics methods; with particular attention to the ULARC junior investigators.

Agency
National Institute of Health (NIH)
Institute
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Type
Specialized Center (P50)
Project #
1P50AA024337-01
Application #
8978011
Study Section
Special Emphasis Panel (ZAA1)
Project Start
2016-05-15
Project End
2021-04-30
Budget Start
2015-07-01
Budget End
2016-06-30
Support Year
1
Fiscal Year
2016
Total Cost
Indirect Cost
Name
University of Louisville
Department
Type
DUNS #
057588857
City
Louisville
State
KY
Country
United States
Zip Code
40208
Hardesty, Josiah E; Al-Eryani, Laila; Wahlang, Banrida et al. (2018) Epidermal Growth Factor Receptor Signaling Disruption by Endocrine and Metabolic Disrupting Chemicals. Toxicol Sci 162:622-634
Yuan, Fuqiang; Chen, Xiaopan; Liu, Jie et al. (2018) Sulforaphane restores acetyl-histone H3 binding to Bcl-2 promoter and prevents apoptosis in ethanol-exposed neural crest cells and mouse embryos. Exp Neurol 300:60-66
Zheng, Yuxuan; Ritzenthaler, Jeffrey D; Burke, Tom J et al. (2018) Age-dependent oxidation of extracellular cysteine/cystine redox state (Eh(Cys/CySS)) in mouse lung fibroblasts is mediated by a decline in Slc7a11 expression. Free Radic Biol Med 118:13-22
Wang, Keling; Chen, Xiaopan; Liu, Jie et al. (2018) Embryonic exposure to ethanol increases the susceptibility of larval zebrafish to chemically induced seizures. Sci Rep 8:1845
Yuan, Fuqiang; Chen, Shao-Yu (2018) Manipulation of MicroRNAs in Cultured Mouse Embryos: Applications for Developmental Toxicology. Methods Mol Biol 1797:205-214
Liang, Yaqin; Lang, Anna L; Zhang, Jian et al. (2018) Exposure to Vinyl Chloride and Its Influence on Western Diet-Induced Cardiac Remodeling. Chem Res Toxicol 31:482-493
Kharbanda, Kusum K; Ronis, Martin J J; Shearn, Colin T et al. (2018) Role of Nutrition in Alcoholic Liver Disease: Summary of the Symposium at the ESBRA 2017 Congress. Biomolecules 8:
Ghosh Dastidar, Shubha; Warner, Jeffrey B; Warner, Dennis R et al. (2018) Rodent Models of Alcoholic Liver Disease: Role of Binge Ethanol Administration. Biomolecules 8:
Gosney, Julie A; Wilkey, Daniel W; Merchant, Michael L et al. (2018) Proteomics reveals novel protein associations with early endosomes in an epidermal growth factor-dependent manner. J Biol Chem 293:5895-5908
Schuster, Susanne; Johnson, Casey D; Hennebelle, Marie et al. (2018) Oxidized linoleic acid metabolites induce liver mitochondrial dysfunction, apoptosis, and NLRP3 activation in mice. J Lipid Res 59:1597-1609

Showing the most recent 10 out of 50 publications