Zinc cooperates with p53 to inhibit the activity of mitochondrial aconitase through reactive oxygen species accumulation
Abstract Metabolic reprogramming is a central hallmark of cancer. Therefore, targeting metabolism may provide an effective strategy for identifying promising drug targets for cancer treatment. In prostate cancer, cells undergo metabolic transformation from zinc‐accumulating, citrate‐producing cells...
Main Authors: | Ya‐Nan Xue, Ya‐Nan Liu, Jing Su, Jiu‐Ling Li, Yao Wu, Rui Guo, Bing‐Bing Yu, Xiao‐Yu Yan, Li‐Chao Zhang, Lian‐Kun Sun, Yang Li |
---|---|
Format: | Article |
Language: | English |
Published: |
Wiley
2019-05-01
|
Series: | Cancer Medicine |
Subjects: | |
Online Access: | https://doi.org/10.1002/cam4.2130 |
Similar Items
-
Aconitase: To Be or not to Be Inside Plant Glyoxysomes, That Is the Question
by: Luigi De Bellis, et al.
Published: (2020-07-01) -
Studying Acetylation of Aconitase Isozymes by Genetic Code Expansion
by: Jessica Araujo, et al.
Published: (2022-03-01) -
Molecular Evolution and Expression Divergence of Aconitase (ACO) Gene Family in Land Plants
by: Yi-ming Wang, et al.
Published: (2016-12-01) -
Loss of mitochondrial aconitase promotes colorectal cancer progression via SCD1-mediated lipid remodeling
by: Xin You, et al.
Published: (2021-06-01) -
The Iron Maiden. Cytosolic Aconitase/IRP1 Conformational Transition in the Regulation of Ferritin Translation and Iron Hemostasis
by: Cécilia Hognon, et al.
Published: (2021-09-01)