Application | Comment | Organism |
---|---|---|
medicine | Caenorhabditis elegans model of the human amyloidogenic disease inclusion body myositis. In a constitutive transgenic Abeta strain that lacks MSRA-1, the number of amyloid aggregates decreases while the number of oligomeric Abeta species increases. The results correlate with enhanced synaptic dysfunction and mislocalization of the nicotinic acetylcholine receptor ACR-16 at the neuromuscular junction | Caenorhabditis elegans |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Caenorhabditis elegans | O02089 | - |
- |
Synonyms | Comment | Organism |
---|---|---|
MSRA-1 | - |
Caenorhabditis elegans |
General Information | Comment | Organism |
---|---|---|
physiological function | Caenorhabditis elegans model of the human amyloidogenic disease inclusion body myositis. In a constitutive transgenic Abeta strain that lacks MSRA-1, the number of amyloid aggregates decreases while the number of oligomeric Abeta species increases. The results correlate with enhanced synaptic dysfunction and mislocalization of the nicotinic acetylcholine receptor ACR-16 at the neuromuscular junction | Caenorhabditis elegans |