Author: Danielle E. Goodman; Carla D. Pretto; Tomas A. Krepostman; Kelly E. Carnahan; Katherine R. Spindler
Title: Enhanced replication of mouse adenovirus type 1 following virus-induced degradation of protein kinase R (PKR) Document date: 2019_3_21
ID: 9utbwy5r_32
Snippet: Instead, we showed that PKR depletion is inhibited by proteasome inhibitors, implicating 315 proteasomal degradation of PKR. Several lines of evidence suggest that the degradation is due to 316 a viral early function. The copyright holder for this preprint (which was not peer-reviewed) is the author/funder. It . https://doi.org/10.1101/584680 doi: bioRxiv preprint antiviral activity during infection (10, 72), MAV-1 does not produce such VA RNAs, .....
Document: Instead, we showed that PKR depletion is inhibited by proteasome inhibitors, implicating 315 proteasomal degradation of PKR. Several lines of evidence suggest that the degradation is due to 316 a viral early function. The copyright holder for this preprint (which was not peer-reviewed) is the author/funder. It . https://doi.org/10.1101/584680 doi: bioRxiv preprint antiviral activity during infection (10, 72), MAV-1 does not produce such VA RNAs, and how 322 MAV-1 infection is affected by PKR is first described in this report. When we infected PKR -/-323 MEFs with MAV-1, viral DNA yields were 5 to 6 times higher than viral DNA yields from wild 324 type MEFs (Fig. 1) , indicating that PKR plays an antiviral role during MAV-1 infection. At 48 325 hpi, the viral DNA yield from the N-MEFs was nearly 4 times higher than the C-MEFs, but by 326 72 hpi the viral DNA yields from both types of PKR -/-MEFs were similar to each other and 327
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