IndraLab

Statements

ATXN3 activates Death. 8 / 8
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"Spinocerebellar ataxia type 3 (SCA3) is the most frequent inherited cerebellar ataxia in Europe, the US and Japan, leading to disability and death through motor complications."
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"These data supported an idea that, due to enhanced interaction to p53 and up-regulation of p53, polyQ expanded ATX-3 led to an increased p53 dependent neuronal cell death (including both early apoptotic and late apoptotic and necrotic manner)."
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"The above results indicate that the expanded polyQ tract in ataxin3 could change the DNA methylation status of a variety of genes involved in various biological processes and, thus, cause neuronal death in the cerebellum and spinal cord due to alterations in the expression of these genes."
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"MJD leads to premature death and there is no therapy available."
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"Taken together, this study provides evidence showing that the truncated ATXN3 accelerates the formation of aggregates, disrupts the dynamics of mitochondria, and leads to neuronal death in vitro and in vivo."
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"It is caused by a CAG over repetition in ATXN3 gene, which translates into a mutated ataxin- 3 protein that accumulates in neurons, causing neuronal dysfunction and death."
| PMC
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"In addition, they found that expanded ataxin3 could activate the mitochondrial apoptotic pathway and induce neuronal death by regulating gene expression [XREF_BIBR]."
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"Spinocerebellar ataxia type 3 (SCA3) is caused by the expansion of a polyglutamine (polyQ) repeat in the protein ataxin-3 which is involved in susceptibility to mild oxidative stress induced neuronal death."
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