Affiliation: Northeastern University
- Age-dependent decrease and alternative splicing of methionine synthase mRNA in human cerebral cortex and an accelerated decrease in autismChristina R Muratore
Department of Pharmaceutical Sciences, School of Pharmacy, Northeastern University, Boston, MA, USA
PLoS ONE 8:e56927. 2013..Factors adversely affecting MS activity, such as oxidative stress, can be a source of risk for neurological disorders across the lifespan via their impact on methylation reactions, including epigenetic regulation of gene expression...
- A macroepigenetic approach to identify factors responsible for the autism epidemic in the United StatesRenee Dufault
Food Ingredient and Health Research Institute, Ocean View, HI, USA
Clin Epigenetics 4:6. 2012....
- How environmental and genetic factors combine to cause autism: A redox/methylation hypothesisRichard Deth
Department of Pharmaceutical Sciences, Northeastern University, Boston, MA 02468, United States
Neurotoxicology 29:190-201. 2008....
- Morphine induces redox-based changes in global DNA methylation and retrotransposon transcription by inhibition of excitatory amino acid transporter type 3-mediated cysteine uptakeMalav Trivedi
Department of Pharmaceutical Sciences, Northeastern University, Boston, Massachusetts M T, J S, N H, R D Center for Molecular Biology and Biotechnology, Florida Atlantic University, Jupiter, Florida R D and Department of Environmental Epidemiology, Harvard School of Public Health, Boston, Massachusetts H M B
Mol Pharmacol 85:747-57. 2014..Since epigenetic changes are implicated in drug addiction and tolerance phenomenon, this study could potentially extrapolate to elucidate a novel mechanism of action for other drugs of abuse. ..
- Soluble oligomers of amyloid-β cause changes in redox state, DNA methylation, and gene transcription by inhibiting EAAT3 mediated cysteine uptakeNathaniel Hodgson
Department of Pharmaceutical Sciences, Northeastern University, Boston, MA 02115, USA
J Alzheimers Dis 36:197-209. 2013..We describe a role of IGF-1 signaling in regulating redox and methylation homeostasis, and propose this to be a pathogenic target of oAβ...