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Abstract
This dissertation uncovers how PARP7 regulates transcription and innate immune signaling, with a focus on its suppression of type I interferon (IFN-I) expression. It identifies the transcriptional coactivators p300 and CBP, as well as IRF3, as key PARP7 substrates, showing that their MARylation drives their degradation or nuclear clearance to repress IFN-I transcription. Additionally, it reveals that PARP7’s own auto-MARylation controls its stability and activity, offering new mechanistic insights and potential therapeutic strategies for enhancing antitumor immunity by targeting PARP7 or its interactions with p300, CBP, and IRF3.