Large-scale screen for modifiers of ataxin-3-derived polyglutamine-induced toxicity in Drosophila.
Polyglutamine (polyQ) diseases represent a neuropathologically heterogeneous group of disorders. The common theme of these disorders is an elongated polyQ tract in otherwise unrelated proteins. So far, only symptomatic treatment can be applied to patients suffering from polyQ diseases. Despite exten...
Main Authors: | Hannes VoSSfeldt, Malte Butzlaff, Katja PrüSSing, Róisín-Ana Ní Chárthaigh, Peter Karsten, Anne Lankes, Sabine Hamm, Mikael Simons, Boris Adryan, Jörg B Schulz, Aaron Voigt |
---|---|
Format: | Article |
Language: | English |
Published: |
Public Library of Science (PLoS)
2012-01-01
|
Series: | PLoS ONE |
Online Access: | http://europepmc.org/articles/PMC3489908?pdf=render |
Similar Items
-
ATAXIN-2 intermediate-length polyglutamine expansions elicit ALS-associated metabolic and immune phenotypes
by: Vieira de Sá, R, et al.
Published: (2024) -
Cross-species genetic screens identify transglutaminase 5 as a regulator of polyglutamine-expanded ataxin-1
by: Won-Seok Lee, et al.
Published: (2022-05-01) -
FTLD-ALS of TDP-43 type and SCA2 in a family with a full ataxin-2 polyglutamine expansion.
by: Bäumer, D, et al.
Published: (2014) -
Ubiquitin-interacting motifs of ataxin-3 regulate its polyglutamine toxicity through Hsc70-4-dependent aggregation
by: Sean L Johnson, et al.
Published: (2020-09-01) -
Nucleocytoplasmic shuttling activity of ataxin-3.
by: Sandra Macedo-Ribeiro, et al.
Published: (2009-06-01)