Background:The function of KAP1 is regulated by multiple posttranslational modifications during DNA damage response. Results: A previously unidentified arginine-rich motif (ARM) of RNF4 regulates the phosphorylation-induced, SUMO-dependent recruitment and degradation of KAP1.
Conclusion:The ARM of RNF4 enhances SIM-SUMO-dependent recruitment. Significance: The bimodular recognition by RNF4 could be critical for fine-tuning substrate selection during DNA damage response and other stress conditions.
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