Adedamola Olayanju

TL;DR: Evidence supporting Keap1-dependent and -independent mechanisms of Nrf2 regulation are dissected, which highlight key knowledge gaps in this important field of biology, and suggest how these may be addressed experimentally.

TL;DR: It is shown that brusatol provokes a rapid and transient depletion of Nrf2 protein, through a posttranscriptional mechanism, in mouse Hepa-1c1c7 hepatoma cells, substantiate brusatols as a useful experimental tool for the inhibition of NRF2 signaling and highlight the potential for therapeutic inhibition ofNrf2 to alter the risk of adverse events by reducing the capacity of nontarget cells to buffer against chemical and oxidative insults.

TL;DR: A comparative iTRAQ-based study in Nrf2(−/−) mice treated with a potent inducer, methyl-2-cyano-3,12-dioxooleana-1,9(11)dien-28-oate (CDDO-me; bardoxolone -methyl), to define both the NRF2-dependent basal and inducible hepatoproteomes and to catalogue the hepatic protein expression profile following acute exposure

TL;DR: A review of the current practices and emerging concepts in safety pharmacology (SP) studies can be found in this article, including frontloading, parallel assessment of core battery studies, use of non-standard species, biomarkers, and combining toxicology and SP assessments.

TL;DR: It is demonstrated that K‐Ras drives UHRF1 expression, establishing a novel link between this oncogene and Nrf2‐mediated cellular protection and suggesting its ability to regulate the Keap1–Nrf2 pathway may be critically important to the malignant behaviour of these cancers.