IndraLab

Statements


ATXN3 activates CHEK1. 6 / 14
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"As mentioned above, ATX3 promotes Chk1 stability through inhibiting its proteasomal destruction."

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"Indeed, overexpression of FBXO6 or DDB1 resulted in significant decrease of Chk1 protein level, whereas co-expression of ATX3 effectively restored Chk1 from E3 ligase mediated degradation."

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"Ataxin-3 promotes genome integrity by stabilizing Chk1."

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"Moreover, ATX3 depleted cells re-entered the cell cycle more rapidly than WT cells did, implying that Chk1 reduction caused by ATX3 knockout can accelerate recovery from the G2/M damage checkpoint, which is consistent with previous results from Chk1-/- ES cells."

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"To test if ATX3 may promote Chk1 stabilization, we first evaluated whether ATX3 deficiency impairs Chk1 stability."

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"Taken together, our results demonstrated that ATX3 promoted Chk1 stability through the ubiquitin-proteasome pathway."