Perspective Open Access
Volume 1 | Issue 1 | DOI: https://doi.org/10.33696/Signaling.1.004
Activation of NLRP3 Inflammosome by N4-Acetyl Cytidine and Its Consequences
Hua Bai1,2,3,*
- 1Department of Neurology, the Third Affiliated Hospital of Guizhou Medical University, China
- 2Department of Neurology, Affiliated Hospital of Guizhou Medical University, China
- 3Medical Experimental Center of the Third Affiliated Hospital of Guizhou Medical University, Duyun, Guizhou 558000, China
Corresponding Author
Hua Bai, 842031616@qq.com
Received Date: February 14, 2020
Accepted Date: April 06, 2020
Bai H. Activation of NLRP3 Inflammosome by N4-Acetyl Cytidine and Its Consequences. J Cell Signal 2020; 1(1):14-17.
Copyright: © 2020 Bai H. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Recommended Articles
Manipulating Oxidative Stress Following Ionizing Radiation
It is now well accepted that the ionizing radiation-generated reactive oxygen species (ROS), that constitute ~2/3 of the effects of external beam radiation, do not only produce direct tumor cell death, but also affect the surrounding microenvironment. Moreover, this indirect effect of radiation may result in systemic effects, specifically the initiation of an inflammatory response.
Activation of NLRP3 Inflammosome by N4-Acetyl Cytidine and Its Consequences
N4-acetylcytidine (N4A) is an organic compound and a metabolite of transferrable ribonucleic acid. Its molecular formula is C11H15N3O6. Earlier studies suggest that N4A was mainly found on tRNA and 18S rRNA, while recent studies have shown that there is also a large amount of N4A on mRNA, whose abundance is not even lower than the m7G cap modification carried by mRNA.
Is Citrate A Critical Signal in Immunity and Inflammation?
When immune cells are activated, they undergo metabolic change in order to have sufficient energy to function effectively. The Krebs cycle is one of the most important pathways involved in this response and citrate, a critical component of this pathway, regulates carbohydrate and lipid metabolism.
Dendorbium Nobile Lindl. Alkaloids Suppress NF-κB and NLRP3 Signaling Pathways to Attenuate Lipopolysaccharide-induced Neuroinflammation
The important immune cells in the brain are called microglia acting as the central junction between neuroinflammation and neurodegenerative diseases. In patients of cognitive disorders and Alzheimer’s disease (AD) animal models, amoebic morphology and inflammatory pathways are activated to release numerous cells in the inflammatory factors by active microglia.
TNFAIP8: Inflammation, Immunity and Human Diseases
Inflammation can be caused by various environmental factors, including microbial infection and toxic chemical exposure. In response to inflammation, immune cells like macrophages, B and T lymphocytes, fibroblasts, endothelial cells, and various stromal cells secrete soluble polypeptide cytokine Tumor Necrosis Factor Alpha (TNF?)