Cargando…
TorsinA rescues ER-associated stress and locomotive defects in C. elegans models of ALS
Molecular mechanisms underlying neurodegenerative diseases converge at the interface of pathways impacting cellular stress, protein homeostasis and aging. Targeting the intrinsic capacities of neuroprotective proteins to restore neuronal function and/or attenuate degeneration represents a potential...
Autores principales: | Thompson, Michelle L., Chen, Pan, Yan, Xiaohui, Kim, Hanna, Borom, Akeem R., Roberts, Nathan B., Caldwell, Kim A., Caldwell, Guy A. |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Company of Biologists Limited
2014
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3917244/ https://www.ncbi.nlm.nih.gov/pubmed/24311730 http://dx.doi.org/10.1242/dmm.013615 |
Ejemplares similares
-
TorsinA participates in endoplasmic reticulum-associated degradation
por: Nery, Flávia C., et al.
Publicado: (2011) -
TorsinA: a therapeutic target for ALS?
Publicado: (2014) -
TorsinA and the TorsinA-Interacting Protein Printor Have No Impact on Endoplasmic Reticulum Stress or Protein Trafficking in Yeast
por: Valastyan, Julie S., et al.
Publicado: (2011) -
TorsinA regulates the LINC to moving nuclei
por: Starr, Daniel A., et al.
Publicado: (2017) -
Resolving the TorsinA Oligomerization Conundrum: The Glycan Hypothesis
por: Fercher, Christian, et al.
Publicado: (2020)