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Evidence for toxic CAG trinucleotide repeats contributing to Huntington’s disease though RNA interference

ABSTRACT: Mutant huntingtin CAG trinucleotide repeat mimetic hairpins are loaded into the RISC and kill cells through RNAi

ORGANISM(S): synthetic construct

PROVIDER: GSE201694 | GEO | 2022/04/27

REPOSITORIES: GEO

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Evidence for toxic CAG trinucleotide repeats contributing to Huntington’s disease though RNA interference

Project description:Mutant huntingtin CAG trinucleotide repeat mimetic hairpins are loaded into the RISC and kill cells through RNAi

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Transcription profiling of mouse cerebellum cells containing expanded or normal CAG trinucleotide repeats in the coding region for TATA-binding protein (TBP)

Project description:Transcription profiles were obtained for 2-month old mice containing an expanded or normal CAG trinucleotide repeat in the coding region for TATA-binding protein (TBP). Three different genotypes were used : TBP-13Q (normal), TBP-71Q (71 repeats), and TBP-105Q (105 repeats). Two lines of TBP-71Q (lines 16 and 27) were used in these experiments. <br><br> The 71Q and 105Q mice express a mutant version of the protein (TBP) and faithfully model the disease SCA17 (spinocerebellar ataxia-17, huntington disease-like 4, HDL4). <br><br> The constructs containing mixed CAG/CAA trinucleotide repeats (and encoding polyglutamine tracts) of variable length were made using a previously described method (Michalik A et al., Biotechniques, 2001). Briefly, synthetic CAG/CAA oligonucleotides were subcloned into a cDNA construct of the normal mouse (13 CAG/CAA) TBP gene. Because of the mixed nature of the repeat, its length is stable in mitotic and meiotic transmission.

2007-11-09 | E-MEXP-1313 | biostudies-arrayexpress