Alzheimer’s disease Aβ42 peptide induces an increase in Na,K-ATPase glutathionylation
- Authors: Lakunina V.A.1, Petrushanko I.Y.1, Burnysheva K.M.1, Mitkevich V.A.1, Makarov A.A.1
-
Affiliations:
- Engelhardt Institute of Molecular Biology
- Issue: Vol 473, No 1 (2017)
- Pages: 114-117
- Section: Biochemistry, Biophysics, and Molecular Biology
- URL: https://journal-vniispk.ru/1607-6729/article/view/211861
- DOI: https://doi.org/10.1134/S1607672917020077
- ID: 211861
Cite item
Abstract
We have shown that the inhibition of Na,K-ATPase during its long-term incubation with amyloid beta (Aβ42), an Alzheimer’s disease protein, is caused by the change in the thiol redox status of cells leading to induction of glutathionylation α-subunit of Na,K-ATPase. To restore the activity of Na,K-ATPase, it is proposed to use reducing agents, which promote normalization of the redox status of cells and deglutathionylation of the protein.
About the authors
V. A. Lakunina
Engelhardt Institute of Molecular Biology
Email: aamakarov@eimb.ru
Russian Federation, Moscow, 119991
I. Y. Petrushanko
Engelhardt Institute of Molecular Biology
Email: aamakarov@eimb.ru
Russian Federation, Moscow, 119991
K. M. Burnysheva
Engelhardt Institute of Molecular Biology
Email: aamakarov@eimb.ru
Russian Federation, Moscow, 119991
V. A. Mitkevich
Engelhardt Institute of Molecular Biology
Email: aamakarov@eimb.ru
Russian Federation, Moscow, 119991
A. A. Makarov
Engelhardt Institute of Molecular Biology
Author for correspondence.
Email: aamakarov@eimb.ru
Russian Federation, Moscow, 119991
Supplementary files
