CIDeRGeneral Information:
| Id: | 1,101 (click here to show other Interactions for entry) |
| Diseases: |
Amyotrophic lateral sclerosis
Huntington disease - [OMIM] |
| Rattus norvegicus | |
| BTO:0001009 PC-12 cell | |
| article | |
| Reference: | Ravikumar B et al.(2005) Dynein mutations impair autophagic clearance of aggregate-prone proteins. Nat. Genet. 37: 771-776 [PMID: 15980862] |
Interaction Information:
| Comment | The authors used stable inducible neuronal precursor cells lines (PC12) that express two different autophagy substrates, a green fluorescent protein (GFP)-tagged mutant huntingtin fragment encoded by exon 1 with 74 glutamine repeats (Q74-GFP) or A53T alpha-synuclein. Clearance of these transgene products is markedly retarded by inhibition of autophagy. Erythro-9-[3-(2-hydroxynonyl)] adenine (EHNA), a dynein inhibitor, slowed turnover of A53T alpha-synuclein and Q74-GFP. EHNA also increased the numbers of PC12 and COS-7 cells with huntingtin aggregates, consistent with impaired clearance of mutant huntingtin. |
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Formal Description Interaction-ID: 6996 |
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| Comment | The authors used stable inducible neuronal precursor cells lines (PC12) that express two different autophagy substrates, a green fluorescent protein (GFP)-tagged mutant huntingtin fragment encoded by exon 1 with 74 glutamine repeats (Q74-GFP) or A53T alpha-synuclein. Clearance of these transgene products is markedly retarded by inhibition of autophagy. Erythro-9-[3-(2-hydroxynonyl)] adenine (EHNA), a dynein inhibitor, slowed turnover of A53T alpha-synuclein and Q74-GFP. EHNA also increased the numbers of PC12 and COS-7 cells with huntingtin aggregates, consistent with impaired clearance of mutant huntingtin. |
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Formal Description Interaction-ID: 6997 |
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