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10.1016/j.molonc.2016.06.002 Mol

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therapy has been developed as a targeted immunomodulatory strategy to specifically correct this Treg cell defect

While typical proteasomal substrates such as CDKN1A (p21), HIF-1, and MCL1 were turned over at short timecourses, the substrates we found as TRIP12/UBR5-co-regulated proteins, including OTUD5, were relatively long-lived proteins (Fig