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ATXN3 activates cell death. 29 / 35
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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 the previous study, downregulation of ATXN3 by its specific siRNA leads to cytoskeletal disorganization as well as focal adhesion defect and increased cell death."
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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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"Indeed, a LOF of brat mitigates neither debcl- (this paper) nor hid- or Sca3 induced cell death [XREF_BIBR]."
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"Co-expression of InR.Exel led to a substantial suppression in the SCA3 induced cell death ( Fig. 5 C, I)."
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"Despite the fact that inclusions are a pathological hallmark of MJD, and high expression of full-length ataxin-3 causes cell death and formation of intranuclear inclusions, there is no clear correlation between the presence of intranuclear inclusions and cell death [153]."
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"Lysine-free ataxin-3 induces cell death via apoptosis."
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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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"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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"Moreover, polyQ-expanded ataxin-3 was shown to exacerbate this physiological process, triggering increased cell death and thereby neurodegeneration (Liu et al., 2016)."
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"An MJD -transfected cell model was used because neurotoxicity in polyQ diseases occurs in a length-dependent manner (47) and our previous studies have reported that the MJD construct induces more severe cell death (22,56)."
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"The expression of MJD alone led to severe cell death when compared with the untransfected control (Figure 6B)."
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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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"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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"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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"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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"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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"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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"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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"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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"Indeed, expression of expanded ataxin-3 alone was sufficient to increase cell death in this model."
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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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"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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"In fact, some cellular models of MJD show decreased antioxidant enzyme activity and increased mitochondrial mediated cell death via apoptosis."
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"Overexpression of expanded ataxin-3 enhances cell death upon mitochondrial complex II inhibition."
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"Absence of ataxin-3 leads to cytoskeletal disorganization and increased cell death."
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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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"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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"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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