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ATXN3 activates TP53. 12 / 18
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"When the FL ATX-3 mRNA was injected into WT but not the p53 mutant zebrafish embryos, significantly more apoptotic cells were observed in TUNEL staining assays, indicating that ATX-3 caused p53 dependent apoptosis in vivo."
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"Using the zebrafish model system, we further examined whether ATX-3 induces p53 dependent apoptosis in vivo."
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"Furthermore, to test whether mutant ATXN3 activates p53 and Chk2 via activating ATM, we pre-treated the cells with ATM inhibitor Ku55933 and expressed ATXN3-Q84 and assessed the activation of DNA damage response pathway."
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"Flow cytometry analysis using Annexin V-FITC and propidium iodide (PI) staining in HCT116 cells showed that knockdown of ATX-3 led to a decrease of camptothecin (CPT)-induced apoptosis, while ectopic expression of ATX-3 but not the catalytic inactive mutant ATX-3-C14A resulted in a significant increase of apoptosis in HCT116 p53 +/+ but not HCT116 p53 -/- cells (XREF_FIG), indicating that ATX-3 promoted p53 mediated apoptosis, which required its deubiquitinating enzymatic activity."
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"As P53 has known functions in cycle arrest and apoptosis, this indicates that expression of atxn3 polyQ repeats induces selective transcription and expression of p53 target genes and promotes p53 dependent apoptosis in the CNS of zebrafish [XREF_BIBR]."
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"ATX-3 Promotes p53 Dependent Apoptosis in Cells and in Zebrafish."
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"Deletion of ATXN3 resulted in destabilization of p53, whereas ectopic expression of ATXN3 induced expression of p53 target genes and promoted p53-dependent apoptosis."
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"The expression levels of p53 responsive genes (such as p21 and Puma) were also higher in ATX-3 exp (80Q) expressing RKO cells (XREF_SUPPLEMENTARY), suggesting that p53 was functionally enhanced by polyQ expansion in ATX-3."
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"Activation of p53 by mutant ataxin-3 is also related to phosphorylation of p53 at ser15 residue in the SCA3 transgenic mice model."
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"Besides, we found that the degradation of p53 in the ATX-3 exp (80Q)-expressing cells was slower than that of normal ATX-3-expressing cells (XREF_SUPPLEMENTARY), and ectopic expression of polyQ expanded ATX-3 induced higher levels of p53 protein than the normal ATX-3 in RKO, 293T, and MEF cells (XREF_SUPPLEMENTARY), indicating that polyQ expanded ATX-3 possessed enhanced capability to stabilize p53."
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"These results suggest that ATX-3 deletion inhibits the stimulation of p53 transactivation activity."
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"However, the polyQ expanded ATX-3 induced progressive severe p53 dependent neurodegeneration in the central nervous system of zebrafish, suggesting that it caused other kinds of p53 mediated neural cell death besides apoptosis, too."
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