
IndraLab
Statements
USP18 inhibits cell death. 5 / 5
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5
reach
"Our results demonstrate that I60N retains deISGylase activity, and the observed accumulation of ISGylated proteins can be decoupled from the loss of catalytic function.Partial impairments in scaffold function by the I60N mutation were correlated with intermediate levels of ISGylation and IFN sensitivity, implicating scaffold function as the primary mechanism by which USP18 loss promotes tumor intrinsic growth arrest and cell death."