J
James J. Galligan
Researcher at University of Arizona
Publications - 41
Citations - 1685
James J. Galligan is an academic researcher from University of Arizona. The author has contributed to research in topics: Oxidative stress & Lipid peroxidation. The author has an hindex of 18, co-authored 41 publications receiving 1321 citations. Previous affiliations of James J. Galligan include University of Colorado Denver & Vanderbilt University Medical Center.
Papers
More filters
Journal ArticleDOI
The human protein disulfide isomerase gene family
TL;DR: Understanding the mechanisms of protein-folding, specifically thiol-disulfide exchange, may lead to development of a novel class of therapeutics that would help alleviate a wide range of diseases by targeting the unfolded protein response.
Journal ArticleDOI
From the exposome to mechanistic understanding of chemical-induced adverse effects
Beate I. Escher,Jörg Hackermüller,Tobias Polte,Stefan Scholz,Achim Aigner,Rolf Altenburger,Alexander Böhme,Stephanie K. Bopp,Werner Brack,Wibke Busch,Marc Chadeau-Hyam,Adrian Covaci,Adolf Eisenträger,James J. Galligan,Natàlia Garcia-Reyero,Thomas Hartung,Michaela Hein,Gunda Herberth,Annika Jahnke,Jos C. S. Kleinjans,Nils Klüver,Martin Krauss,Marja H. Lamoree,Irina Lehmann,Till Luckenbach,Gary W. Miller,Andrea Müller,David H. Phillips,Thorsten Reemtsma,Ulrike Rolle-Kampczyk,Gerrit Schüürmann,Benno Schwikowski,Yu Mei Tan,Saskia Trump,Susanne Walter-Rohde,John F. Wambaugh +35 more
TL;DR: If mechanistic understanding of the causal links between exposure and adverse effects on human health and the environment can be improved by integrating the exposome approach with the adverse outcome pathway (AOP) concept, this work explores whether this concept can be extended to include broader ecological issues.
Journal ArticleDOI
Overview of lipid peroxidation products and hepatic protein modification in alcoholic liver disease
TL;DR: Inhibition of Hsp70, Hsp90 and PDI function could be involved in initiation of the early phases of ER stress contributing to stimulation and accumulation of hepatic lipids and disruption of lipid transport also contributing to steatosis.
Journal ArticleDOI
Mitochondrial Acetylome Analysis in a Mouse Model of Alcohol-Induced Liver Injury Utilizing SIRT3 Knockout Mice
TL;DR: Overall increases in 91 mitochondrial targets for protein acetylation are revealed, identifying numerous critical metabolic and antioxidant pathways associated with ALD, suggesting an important role for mitochondrial proteinacetylation in the pathogenesis of ALD.
Journal ArticleDOI
4-Hydroxynonenal inhibits SIRT3 via thiol-specific modification.
Kristofer S. Fritz,James J. Galligan,Rebecca L. Smathers,James R. Roede,Colin T. Shearn,Philip Reigan,Dennis R. Petersen +6 more
TL;DR: Computer-based molecular modeling simulations indicate that 4-HNE modification alters the conformation of the zinc-binding domain inducing minor changes within the active site, resulting in the allosteric inhibition of SIRT3 activity.