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John F. Reichard

Researcher at University of Cincinnati

Publications -  33
Citations -  2247

John F. Reichard is an academic researcher from University of Cincinnati. The author has contributed to research in topics: Aryl hydrocarbon receptor & Medicine. The author has an hindex of 18, co-authored 29 publications receiving 1942 citations. Previous affiliations of John F. Reichard include Icahn School of Medicine at Mount Sinai & Anschutz Medical Campus.

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Heme oxygenase-1 induction by NRF2 requires inactivation of the transcriptional repressor BACH1

TL;DR: BACH1 confers an additional level of regulation to ARE-dependent genes that reveals a new dimension to the oxidative stress response and is compared with thioredoxin reductase 1.
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The Library of Integrated Network-Based Cellular Signatures NIH Program: System-Level Cataloging of Human Cells Response to Perturbations

Alexandra B Keenan, +107 more
- 29 Nov 2017 - 
TL;DR: The LINCS program focuses on cellular physiology shared among tissues and cell types relevant to an array of diseases, including cancer, heart disease, and neurodegenerative disorders.
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Effects of arsenic exposure on DNA methylation and epigenetic gene regulation

TL;DR: The evidence supporting changes in DNA methylation as a cause of arsenic carcinogenesis is discussed and the strengths and limitations of these studies are highlighted, as well as areas where consistencies and inconsistencies exist.
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Long term low-dose arsenic exposure induces loss of DNA methylation.

TL;DR: It is found that arsenic causes the depletion of S-adenosylmethionine, the main cellular methyl donor, and represses the expression of the DNA methyltransferase genes DNMT1 and DNMT3A, and possibly as a consequence of these two complementary mechanisms, long-term exposure to arsenic results in DNA hypomethylation.
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4-Hydroxynonenal and Malondialdehyde Hepatic Protein Adducts in Rats Treated with Carbon Tetrachloride: Immunochemical Detection and Lobular Localization

TL;DR: Results demonstrate that 4-HNE and MDA alkylate specific hepatic proteins in a time-dependent manner, which appears to be associated with hepatocellular injury following CCl(4) exposure.