TAK1 Mediates ROS Generation Triggered by the Specific Cephalosporins through Noncanonical Mechanisms.
Animals
Anti-Bacterial Agents
/ pharmacology
Blotting, Western
Cefotaxime
/ pharmacology
Cell Survival
/ drug effects
Cephalosporins
/ pharmacology
MAP Kinase Kinase Kinase 5
/ metabolism
MAP Kinase Kinase Kinases
/ genetics
Macrophages
/ drug effects
Membrane Potential, Mitochondrial
/ drug effects
Mice
Mice, Knockout
Mitogen-Activated Protein Kinases
/ metabolism
Oxidative Stress
/ drug effects
RAW 264.7 Cells
Reactive Oxygen Species
/ metabolism
Signal Transduction
/ drug effects
antibacterial agents
macrophages
reactive oxygen species (ROS)
transforming growth factor-β (TGF-β)-activated kinase 1 (TAK1)
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
14 Dec 2020
14 Dec 2020
Historique:
received:
13
11
2020
revised:
11
12
2020
accepted:
12
12
2020
entrez:
17
12
2020
pubmed:
18
12
2020
medline:
16
3
2021
Statut:
epublish
Résumé
It is known that a wide variety of antibacterial agents stimulate generation of reactive oxygen species (ROS) in mammalian cells. However, its mechanisms are largely unknown. In this study, we unexpectedly found that transforming growth factor-β (TGF-β)-activated kinase 1 (TAK1) is involved in the generation of mitochondrial ROS (mtROS) initiated by cefotaxime (CTX), one of specific antibacterial cephalosporins that can trigger oxidative stress-induced cell death. TAK1-deficient macrophages were found to be sensitive to oxidative stress-induced cell death stimulated by H
Identifiants
pubmed: 33327477
pii: ijms21249497
doi: 10.3390/ijms21249497
pmc: PMC7764951
pii:
doi:
Substances chimiques
Anti-Bacterial Agents
0
Cephalosporins
0
Reactive Oxygen Species
0
Mitogen-Activated Protein Kinases
EC 2.7.11.24
MAP Kinase Kinase Kinase 5
EC 2.7.11.25
MAP Kinase Kinase Kinases
EC 2.7.11.25
MAP kinase kinase kinase 7
EC 2.7.11.25
Map3k5 protein, mouse
EC 2.7.11.25
Cefotaxime
N2GI8B1GK7
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
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