IndraLab

Statements



reach
"We identified that nuclear USP18 diminishes binding of IFN regulated transcription factors to their corresponding DNA motifs in cooperation with NF-κB. Consequently, the suppression of USP18 not only enhances the expression of canonical IFN-stimulated genes (ISGs) but also activates a set of atypical ISGs and NF-κB target genes that induce cancer pyroptosis."

reach
"Knockdown of USP18 represses the transcription factor PML and RARalpha and inhibits growth of acute promyelocytic leukaemia [24]."

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"Nuclear USP18 cooperates with NF-κB to reduce the binding of IFN-regulated transcription factors to their corresponding DNA motifs."

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"Silencing USP18 prolongs the phosphorylated state of signal transducer and activator of transcription 1 (STAT1) and enhances the expression of ISGs in response to IFN-alpha [XREF_BIBR]."

reach
"Our genome wide analyses reveal that nuclear USP18 diminishes binding of IFN-regulated transcription factors to their corresponding DNA motifs in cooperation with NF-κB."