Mar 1, 2021 · By using antioxidants N-acetylcysteine and catalase, we found that ERK pathway was activated by a reactive oxygen species- (ROS-) dependent mechanism after exposure to urinary proteins.

Jan 13, 2021 · Our data demonstrate new relationships between regeneration-related ROS production and MAPK/ERK activation at the earliest regeneration stages, as well as the involvement of the...

Activated ERK1/2 phosphorylates RSK and both RSK and ERK translocate to the nucleus where they activates multiple transcription factors ultimately resulting in effector protein synthesis and causing changes in cell proliferation and survival.

Jun 23, 2020 · The core RAS–ERK pathway is typically initiated at the plasma membrane, where guanosine triphosphate (GTP)-loaded RAS directly contacts the RAF kinases and induces catalytic activity through...

Feb 1, 2024 · Reactive oxygen species (ROS) activate JNK, p38 and ERK mitogen-activated protein kinases (MAPK), which upregulate c-Jun and c-Fos expression at the transcriptional level.

Dec 4, 2021 · Studies have confirmed that higher concentrations of ROS leads to autophagy or cell death. In this research, the role of CC90003-induced ROS was verified. But after inhibiting ROS by two...

ROS and the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway were inhibited to detect the MAPK/ERK pathway, nuclear factor erythroid factor 2-related factor 2 (Nrf2), hypoxia-inducible factor-1α (Hif-1α), and interleukin-17D (IL …

Mar 2, 2021 · Urinary protein-induced ROS production triggers a cascade of phosphorylation reactions in the ERK pathway, which is a common mediator of protective autophagy and injury in TECs.

One type of stress that induces potential activation of MAPK pathways is the oxidative stress caused by reactive oxygen species (ROS). Generally, increased ROS production in a cell leads to the activation of ERKs, JNKs, or p38 MAPKs, but the mechanisms by which ROS can activate these kinases are unclear.

For example, ROS can stimulate ERK signaling via activation of upstream activators and inactivation of catalytic activity of DUSPs, which leads to sustained ERK activation due to the lack of negative feedback responses elicited by DUSPs.