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ETO/CTH‐induced DNA damage appears to promote a p53/p21‐dependent pathway. This is associated with cell cycle arrest, evidenced by decrease in MCM2 expression. Furthermore, CDK1—responsible for SAMHD1 phosphorylation—is downregulated. As a result, SAMHD1 is not phosphorylated and becomes active against HIV‐1 infection. Dephosphorylated, active SAMHD1 induced by DNA damage appears to block 2LTR and provirus formation.
