IndraLab

Statements

FBXL3 inhibits ATXN3. 5 / 5
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"While the specific mechanism by which FBXL3 mediates reduction of ATXN3 abundance remains to be defined, the development of small molecules that activate this mechanism could be of therapeutic value for SCA3."
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"To evaluate if FBXL3 mediated reduction of ATXN3 abundance occurs via the SCF and CUL1 ubiquitination complex, we co-electroporated plasmid overexpressing FBXL3 while also decreasing CUL1 with siRNAs against CUL1 (XREF_FIG)."
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"If FBXL3 knockdown increases ATXN3 abundance, then its overexpression would be expected to decrease ATXN3 protein levels."
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"Knockdown of CUL1 abolished FBXL3 mediated reduction of normal ATXN3, but only accounted for about half of the observed FBXL3 facilitated decrease of pathogenic ATXN3 (XREF_FIG), suggesting that FBXL3 handles or recognizes normal and mutant ATXN3 differently."
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"Overexpression of FBXL3 suppresses ATXN3 abundance in a CUL1 dependent manner in SCA3 neuronal progenitor cells (NPCs)."
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