IndraLab

Statements


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"Among identified candidates were known regulators of IFN signaling such as Usp25 ( Lin et al., 2015 ), Usp15 ( Pauli et al., 2014 ), and DUBA, which displayed reduced expression in H1N1-infected cells[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"In addition, we demonstrated that in contrast to USP15 de-ubiquitinating (DUB) activity, USP15 mediated inhibition of IFN signaling was not abolished by mutations eliminating the catalytic activity, indicating that a fraction of USP15 mediated IFN antagonism was independent of the DUB activity."

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"Knockdown of USP15 results in upregulation of type I IFN."

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"In addition, the ectopic expression of USP15 enhances the TRIM25- and RIG-I-mediated production of type I IFN and thus suppresses RNA virus replication, whereas the depletion of USP15 causes decreased IFN production and markedly enhanced viral replication (85)."

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"Furthermore, ectopic expression of USP15 enhanced the TRIM25- and RIG-I-dependent production of type I IFN and suppressed RNA virus replication."

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"Among these proteins, we found Ubiquitin carboxyl-terminal hydrolase 15 (Usp15) which positively regulates type I interferon responses and thereby antiviral immune response."