Mónica Báñez-Coronel
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View article: Repeat associated non-AUG translation as a common mechanism for the polyGln ataxias
Repeat associated non-AUG translation as a common mechanism for the polyGln ataxias Open
Determining if repeat associated non-AUG (RAN) proteins contribute to the CAG polyGln-encoding spinocerebellar ataxias (CAG-SCAs) is critical for understanding mechanisms and developing therapies for these diseases. Immunohistochemistry us…
View article: <i>CASP8</i> intronic expansion identified by poly-glycine-arginine pathology increases Alzheimer’s disease risk
<i>CASP8</i> intronic expansion identified by poly-glycine-arginine pathology increases Alzheimer’s disease risk Open
Alzheimer’s disease (AD) affects more than 10% of the population ≥65 y of age, but the underlying biological risks of most AD cases are unclear. We show anti-poly-glycine-arginine (a-polyGR) positive aggregates frequently accumulate in spo…
View article: CCG•CGG interruptions in high penetrance SCA8 families increase RAN translation and protein toxicity
CCG•CGG interruptions in high penetrance SCA8 families increase RAN translation and protein toxicity Open
Spinocerebellar ataxia type 8 (SCA8), a dominantly inherited neurodegenerative disorder caused by a CTG•CAG expansion, is unusual because most individuals that carry the mutation do not develop ataxia. To understand the variable penetrance…
View article: Targeting CAG repeat RNAs reduces Huntington’s disease phenotype independently of huntingtin levels
Targeting CAG repeat RNAs reduces Huntington’s disease phenotype independently of huntingtin levels Open
Huntington's disease (HD) is a polyglutamine disorder caused by a CAG expansion in the Huntingtin (HTT) gene exon 1. This expansion encodes a mutant protein whose abnormal function is traditionally associated with HD pathogenesis; however,…