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_2
Snippet: The first line of defense in cells during viral infection is the innate immune system, which 44 is activated by different viral products. PKR is a part of this innate immune system and is 45 induced by interferon and activated by dsRNA produced by DNA and RNA viruses. PKR is such 46 discovered that the PKR -/-MEF lines used are not complete PKR knockouts (52). There are two 116 categories of PKR -/-MEFs derived from knockout mice: N-PKR -/-MEFs a.....
Document: The first line of defense in cells during viral infection is the innate immune system, which 44 is activated by different viral products. PKR is a part of this innate immune system and is 45 induced by interferon and activated by dsRNA produced by DNA and RNA viruses. PKR is such 46 discovered that the PKR -/-MEF lines used are not complete PKR knockouts (52). There are two 116 categories of PKR -/-MEFs derived from knockout mice: N-PKR -/-MEFs and C-PKR -/-MEFs 117 (52). The PKR -/-MEFs derived from mice created in the Weissmann lab (53) are designated N-118 PKR -/-MEFs, because the C-terminal fragment of PKR is still expressed and can be detected by 119 immunoblot when there is IFN induction (52). The fragment has the kinase catalytic activity of 120 PKR, but it does not bind dsRNA (52). The PKR -/-MEFs derived from mice created in the Bell 121 lab (54) are designated as C-PKR -/-MEFs, because the N-terminal fragment of PKR is still 122 expressed and can be detected by immunoblot with specific PKR antibodies (52). The fragment 123 is catalytically inactive, but it can still bind dsRNA (52). Susceptibility of these PKR -/-MEFs to 124 specific viruses may be dependent on the PKR mutation and the mechanism used by each virus 125 to circumvent PKR. 126
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