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ATXN3 activates cell death. 23 / 29
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"Here, we report on the potential use of lithium carbonate and coenzyme Q10 (CoQ10) to reduce the cell death caused by the expanded ATX3 in a cultured cell model."
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"The truncated form of mutated ataxin-3 causes aggregation and cell death in vitro and in vivo."
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"Our observation demonstrated that the degradation of Hsp27 in SK-N-SH cells is not mediated by the proteasome degradation pathway.We have previously shown that expanded ataxin-3 leads to an increased [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Here, we report on the potential use of lithium carbonate and coenzyme Q10 to reduce cell death caused by the expanded ATX3 in cell culture."
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"For example, an expansion of the polyglutamine tract of the ataxin-3 protein, the target protein of SCA3, can lead to decreased Bcl-2 expression and enhance cell death via mitochondria dependent apopt[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Previously, it was shown that ataxin-3 is localized in the cytoplasmic compartment of cells and that expression of ataxin-3 with polyglutamine expansions causes cell death XREF_BIBR XREF_BIBR XREF_BIBR XREF_BIBR."
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"In fact, some cellular models of MJD show decreased antioxidant enzyme activity and increased mitochondrial mediated cell death via apoptosis."
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"Nevertheless, much remains unknown about how the CAG expansion in the ATXN3 gene causes brain dysfunction and cell death, manifesting in a characteristic clinical syndrome."
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"Indeed, a LOF of brat mitigates neither debcl- (this paper) nor hid- or Sca3 induced cell death [XREF_BIBR]."
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"In a SCA 3 cell model, the expression of a fragment of ataxin-3 containing an elongated polyQ stretch induced apoptosis and cell death as well as a severe ataxia in a mouse model, showing a more rapid manifestation of a SCA 3-reminiscent phenotype when compared to mice expressing full length mutant ataxin-3 [XREF_BIBR]."
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"High level expression of expanded full-length ataxin-3 in vitro causes cell death and formation of intranuclear inclusions in neuronal cells."
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"A LDH assay has been applied for evaluating peptide efficacy in inhibiting cell death induced by MJD CAG78 in HEK293 cells [XREF_BIBR]."
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"Transient expression of full-length expanded ATX3 (Q84) induced intracellular aggregate formation and cell death when compared with cells expressing constructs with normal ATX3 (Q28), as previously demonstrated."
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"Furthermore, although high level expression of expanded full-length ataxin-3 in vitro causes cell death and formation of NIIs in neurones, there is no close correlation between cell death and NIIs [18[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Ikeda et al. 1996 showed that a short fragment of the MJD1 protein containing 79 polyglns (Q79C) but not the full-length protein with the elongated repeat induced apoptotic cell death in COS cells."
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"In our study, we found that expression of different ataxin-3 constructs in HEK293 T cells caused repeat length dependent cell death."
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"We explored the protective effects of the compatible solutes ectoine, hydroxyectoine, and betaine on apoptotic cell death produced by the truncated MJD gene product with an expanded polyglutamine tract in cultured neuro2a cells."
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"Overexpression of expanded ataxin-3 enhances cell death upon mitochondrial complex II inhibition."
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"Even though no degenerative phenotype was observed either in a MJD knockout animal XREF_BIBR or upon non specific gene silencing in a lentiviral rat model XREF_BIBR, absence of ataxin-3 has been reported to mediate cytoskeletal disorganization and increase cell death in cellular lines XREF_BIBR."
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"Absence of ataxin-3 leads to cytoskeletal disorganization and increased cell death."
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"On one hand, MJD/SCA-3 is an inherited neurodegenerative disorder where the truncated form of mutated ataxin-3 causes aggregation and cell death in vitro and in vivo."
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"Indeed, expression of expanded ataxin-3 alone was sufficient to increase cell death in this model."
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"Downregulation of ATXN3 enhanced AKT inhibitors (perifosine or MK-2206) induced cell death by BIM, but decreased the cell death induced by chemotherapeutic drugs (etoposide or cisplatin) via Bcl-xl."
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