Carregando...
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...
Na minha lista:
| Principais autores: | , |
|---|---|
| Formato: | Artigo |
| Idioma: | Inglês |
| Publicado em: |
The Rockefeller University Press
2005
|
| Assuntos: | |
| Acesso em linha: | https://ncbi.nlm.nih.gov/pmc/articles/PMC2171781/ https://ncbi.nlm.nih.gov/pubmed/15767459 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1083/jcb.200411026 |
| Tags: |
Adicionar Tag
Sem tags, seja o primeiro a adicionar uma tag!
|