Upon oxidative stress, sensor cysteines in Keap1 are modified by ROS, leading to Nrf2 stabilization, accumulation, and translocation to the nucleus where Nrf2 heterodimerizes with sMaf and binds to the ARE to activate the transcription of antioxidant genes.

Accumulating evidence has shown that mitochondrial ROS (mtROS) activate Nrf2, often mediated by certain protein kinases, and induce the expression of antioxidant genes and genes involved in mitochondrial quality/quantity control.

Feb 17, 2020 · Accumulating evidence has shown that mitochondrial ROS (mtROS) activate Nrf2, often mediated by certain protein kinases, and induce the expression of antioxidant genes and genes involved in mitochondrial quality/quantity control.

We here show that ROS production in Nrf2-KO cells and tissues is increased compared to their WT counterparts. Mitochondrial ROS production is regulated by the Keap1–Nrf2 pathway by controlling mitochondrial bioenergetics.

Nov 27, 2022 · This review aims to provide the reader with a general overview of oxidative stress and Nrf2, including basic mechanisms of Nrf2 activation and regulation, and implications in various major human diseases.

Jan 1, 2020 · Our data show that ROS, KRAS and Nrf2 form a molecular axis preventing ROS accumulation to toxic levels that could inhibit proliferation. We also found that the ROS/KRAS/Nrf2 axis intersects with survival and apoptosis pathways.

Nov 6, 2024 · ROS-sensing Nrf2 inhibits the anti-tumor T cell responses, indicating that Nrf2 may be a potential target for T cell immunotherapy strategies against solid tumors.

Feb 17, 2020 · Accumulating evidence has shown that mitochondrial ROS (mtROS) activate Nrf2, often mediated by certain protein kinases, and induce the expression of antioxidant genes and genes involved in mitochondrial quality/quantity control.

Apr 8, 2025 · After X-ray irradiation, salidroside inhibits the Nuclear factor erythroid 2-like 2 (Nrf2)protein expression and blocks cells in the G2/M phase with the highest radiosensitivity, which amplifies the reactive oxygen species (ROS) generation to exacerbate DNA damage, thus achieving radiosensitization.

The induction of many cytoprotective enzymes in response to ROS is mediated by antioxidant response elements (ARE), which activate the nuclear factor erythroid 2-related factor (Nrf2). ARE is a cis-acting enhancer locating in the 5’ flanking region of many phase II detoxification genes.