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Discussion In the present study, we explored the role of PARP-1 in HCMV infection and found that HCMV infection activated PARP-1 and increased protein PARylation as early as 12 hpi (Figure 2A,B)

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Response of a neuronal model of tuberous sclerosis to mammalian target of rapamycin (mTOR) inhibitors: effects on mTORC1 and Akt signaling lead to improved survival and function