Parkin is a disease modifier in the mutant SOD1 mouse model of ALS
Abstract Mutant Cu/Zn superoxide dismutase (SOD1) causes mitochondrial alterations that contribute to motor neuron demise in amyotrophic lateral sclerosis (ALS). When mitochondria are damaged, cells activate mitochondria quality control (MQC) mechanisms leading to mitophagy. Here, we show that in th...
Main Authors: | Gloria M Palomo, Veronica Granatiero, Hibiki Kawamata, Csaba Konrad, Michelle Kim, Andrea J Arreguin, Dazhi Zhao, Teresa A Milner, Giovanni Manfredi |
---|---|
Format: | Article |
Language: | English |
Published: |
Wiley
2018-10-01
|
Series: | EMBO Molecular Medicine |
Subjects: | |
Online Access: | https://doi.org/10.15252/emmm.201808888 |
Similar Items
-
Mitochondrial Transport and Turnover in the Pathogenesis of Amyotrophic Lateral Sclerosis
by: Veronica Granatiero, et al.
Published: (2019-05-01) -
ALS-Related Mutant SOD1 Aggregates Interfere with Mitophagy by Sequestering the Autophagy Receptor Optineurin
by: Yeong Jin Tak, et al.
Published: (2020-10-01) -
Multitasking guardian of mitochondrial quality: Parkin function and Parkinson’s disease
by: Iryna Kamienieva, et al.
Published: (2021-01-01) -
Decrease of Cardiac Parkin Protein in Obese Mice
by: Amandine Thomas, et al.
Published: (2020-01-01) -
Mitophagy Modulation, a New Player in the Race against ALS
by: Enrique Madruga, et al.
Published: (2021-01-01)