Soona Shin

TL;DR: This review highlights recent observations on the molecular interactions and their functional consequences between NRF2 and the arylhydrocarbon receptor (AhR), NF-κB, p53, and Notch1 signaling pathways, which provide a multi-tiered, integrated response to chemical stresses.

TL;DR: NRF2 regulates expression of Ahr and subsequently modulates several downstream events of the AHR signaling cascade, including inhibition of adipogenesis in mouse embryonic fibroblasts (MEFs) and bidirectional interactions of these pathways.

TL;DR: It is indicated that CDDO-Im is an exceedingly potent agent for preventing obesity, and the Nrf2 pathway is identified as a novel target for management of obesogenesis.

TL;DR: Analysis of pharmacologic activation suggests that Nrf2 is the primary mediator of CDDO-Im activity, though other cell-signaling targets are also modulated following an oral dose of 30 micromol/kg.

TL;DR: Killing Foxl1+ cells by diphtheria toxin administration led to an abrupt cessation of proliferation of both epithelial stem- and transit-amplifying progenitor cell populations that was associated with a loss of active Wnt signaling to the intestinal epithelium, therefore, Foxl 1-expressing mesenchymal cells constitute the fundamental niche for intestinal stem cells.