Cargando…
The AAA+ protein torsinA interacts with a conserved domain present in LAP1 and a novel ER protein
A glutamic acid deletion (ΔE) in the AAA+ protein torsinA causes DYT1 dystonia. Although the majority of torsinA resides within the endoplasmic reticulum (ER), torsinA binds a substrate in the lumen of the nuclear envelope (NE), and the ΔE mutation enhances this interaction. Using a novel cell-based...
| Autores principales: | , |
|---|---|
| Formato: | Texto |
| Lenguaje: | English |
| Publicado: |
The Rockefeller University Press
2005
|
| Materias: | |
| Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2171781/ https://www.ncbi.nlm.nih.gov/pubmed/15767459 http://dx.doi.org/10.1083/jcb.200411026 |