- 【Updated on May 12, 2025】 Integration of CiNii Dissertations and CiNii Books into CiNii Research
- Trial version of CiNii Research Knowledge Graph Search feature is available on CiNii Labs
- 【Updated on June 30, 2025】Suspension and deletion of data provided by Nikkei BP
- Regarding the recording of “Research Data” and “Evidence Data”
ROS and ROS‐Mediated Cellular Signaling
Search this article
Description
<jats:p>It has long been recognized that an increase of reactive oxygen species (ROS) can modify the cell‐signaling proteins and have functional consequences, which successively mediate pathological processes such as atherosclerosis, diabetes, unchecked growth, neurodegeneration, inflammation, and aging. While numerous articles have demonstrated the impacts of ROS on various signaling pathways and clarify the mechanism of action of cell‐signaling proteins, their influence on the level of intracellular ROS, and their complex interactions among multiple ROS associated signaling pathways, the systemic summary is necessary. In this review paper, we particularly focus on the pattern of the generation and homeostasis of intracellular ROS, the mechanisms and targets of ROS impacting on cell‐signaling proteins (NF‐<jats:italic>κ</jats:italic>B, MAPKs, Keap1‐Nrf2‐ARE, and PI3K‐Akt), ion channels and transporters (Ca<jats:sup>2+</jats:sup> and mPTP), and modifying protein kinase and Ubiquitination/Proteasome System.</jats:p>
Journal
-
- Oxidative Medicine and Cellular Longevity
-
Oxidative Medicine and Cellular Longevity 2016 (1), 4350965-, 2016-01
Wiley
- Tweet
Details 詳細情報について
-
- CRID
- 1360855568755500928
-
- ISSN
- 19420994
- 19420900
-
- Data Source
-
- Crossref