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Shota Shibata

As seen in: Nature, BioRxiv
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Articles

Base editing of trinucleotide repeats that cause Huntington’s disease and Friedreich’s ataxia reduces somatic repeat expansions in patient cells and in mice | Nature Genetics

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By Mandana Arbab, Alvin Hsu, Ben Weisburd, Shota Shibata, Liam G Fearnley, Melanie Bahlo, Heidi Rehm, Guangping Gao, Ricardo PInto, Zaneta Matuszek
| Nature Verified
Abstract Trinucleotide repeat (TNR) diseases are neurological disorders caused by expanded genomic TNRs that become unstable in a length-dependent manner. The CAG•CTG sequence is found in approximately one-third of pathogenic TNR loci, including the HTT gene that causes Huntington’s disease. Friedreich’s ataxia, the most prevalent hereditary ataxia, results from GAA repeat expansion at the FXN gene.
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In vivo CRISPR–Cas9 genome editing in mice identifies genetic modifiers of somatic CAG repeat instability in Huntington’s disease - Nature Genetics

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By Ricardo PInto, Cameron Douglas, Shota Shibata, Marion J. Riggs, James F. Gusella
| Nature Verified
Abstract Huntington’s disease, one of more than 50 inherited repeat expansion disorders1, is a dominantly inherited neurodegenerative disease caused by a CAG expansion in HTT2. Inherited CAG repeat length is the primary determinant of age of onset, with human genetic studies underscoring that the disease is driven by the CAG length-dependent propensity of the repeat to further expand in the brain3,4,5,6,7,8,9.
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Splice modulators target PMS1 to reduce somatic expansion of the Huntington’s disease-associated CAG repeat - Nature Communications

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By Dadi Gao, Shota Shibata, Elisabetta Morini, Benjamin P. Kleinstiver, Jong-Min Lee, Ricardo PInto, Iris N. Farnum
| Nature Verified
Abstract Huntington’s disease (HD) is a dominant neurological disorder caused by an expanded HTT exon 1 CAG repeat that lengthens huntingtin’s polyglutamine tract. Lowering mutant huntingtin has been proposed for treating HD, but genetic modifiers implicate somatic CAG repeat expansion as the driver of onset.
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