Polyglutamine Repeats in Viruses
نویسندگان
چکیده
منابع مشابه
Large Polyglutamine Repeats Cause Muscle Degeneration in SCA17 Mice.
In polyglutamine (polyQ) diseases, large polyQ repeats cause juvenile cases with different symptoms than those of adult-onset patients, who carry smaller expanded polyQ repeats. The mechanisms behind the differential pathology mediated by different polyQ repeat lengths remain unknown. By studying knockin mouse models of spinal cerebellar ataxia-17 (SCA17), we found that a large polyQ (105 gluta...
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The polyglutamine diseases are caused in part by a gain-of-function mechanism of neuronal toxicity involving protein conformational changes that result in the formation and deposition of β-sheet rich aggregates. Recent evidence suggests that the misfolding mechanism is context-dependent, and that properties of the host protein, including the domain architecture and location of the repeat tract,...
متن کاملEvolution and function of CAG/polyglutamine repeats in protein–protein interaction networks
Expanded runs of consecutive trinucleotide CAG repeats encoding polyglutamine (polyQ) stretches are observed in the genes of a large number of patients with different genetic diseases such as Huntington's and several Ataxias. Protein aggregation, which is a key feature of most of these diseases, is thought to be triggered by these expanded polyQ sequences in disease-related proteins. However, p...
متن کاملCaspase-8 Is Required for Cell Death Induced by Expanded Polyglutamine Repeats
We show here that caspase-8 is required for the death of primary rat neurons induced by an expanded polyglutamine repeat (Q79). Expression of Q79 recruited and activated caspase-8. Inhibition of caspase-8 blocked polyglutamine-induced cell death. Coexpression of Q79 with the caspase inhibitor CrmA, a dominant-negative mutant of FADD (FADD DN), Bcl-2, or Bcl-xL, but not an N-terminally tagged Bc...
متن کاملPolyglutamine Repeats Are Associated to Specific Sequence Biases That Are Conserved among Eukaryotes
Nine human neurodegenerative diseases, including Huntington's disease and several spinocerebellar ataxia, are associated to the aggregation of proteins comprising an extended tract of consecutive glutamine residues (polyQs) once it exceeds a certain length threshold. This event is believed to be the consequence of the expansion of polyCAG codons during the replication process. This is in appare...
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ژورنال
عنوان ژورنال: Molecular Neurobiology
سال: 2018
ISSN: 0893-7648,1559-1182
DOI: 10.1007/s12035-018-1269-4