IndraLab

Statements


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"Altogether, these results further support our findings that ATX3 selectively fine‐tunes DSB repair by preventing extensive RNF8/K63‐ubiquitin signalling, which balances DSB repair pathway choice.Finally, if this model is correct, then removal of RNF8 in ATX3‐depleted cells should prevent excessive 5′‐DNA end resection and restore cell survival after IR."

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"Based on recent studies, we suggest that wildtype ATXN3 stabilizes, or regulates, proteins at various step of the DDR process to promote efficient repair and cell survival."