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E 6x coverage mammalian genomes were used to build a profile hidden Markov model with the software HMMER [81], which was then used to screen the platypus ab initio peptide predictions available from Ensembl. An inferred ancestral HIN domain sequence from the node that predates the split between HIN-A, -B and -C domains was also used to perform this search. The genomes of chicken (Gallus gallus rel
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E 6x coverage mammalian genomes were used to build a profile hidden Markov model with the software HMMER [81], which was then used to screen the platypus ab initio peptide predictions available from Ensembl. An inferred ancestral HIN domain sequence from the node that predates the split between HIN-A, -B and -C domains was also used to perform this search. The genomes of chicken (Gallus gallus rel
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E 6x coverage mammalian genomes were used to build a profile hidden Markov model with the software HMMER [81], which was then used to screen the platypus ab initio peptide predictions available from Ensembl. An inferred ancestral HIN domain sequence from the node that predates the split between HIN-A, -B and -C domains was also used to perform this search. The genomes of chicken (Gallus gallus rel
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By vIF2a or E3L, but not by K3L (Figure 4C). Thus in accord with the virus host range vIF2a, but not VACV K3L, may have evolved to inhibit fish PKR. To assess the effectiveness of K3, E3, and vIF2a to inhibit human and zebrafish PKR, matching sets of strains expressing a particular inhibitor and either no PKR, human PKR, or zebrafish PKR were streaked on the same plate for comparison. Examining th
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By vIF2a or E3L, but not by K3L (Figure 4C). Thus in accord with the virus host range vIF2a, but not VACV K3L, may have evolved to inhibit fish PKR. To assess the effectiveness of K3, E3, and vIF2a to inhibit human and zebrafish PKR, matching sets of strains expressing a particular inhibitor and either no PKR, human PKR, or zebrafish PKR were streaked on the same plate for comparison. Examining th
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R, K3L or vIF2a, demonstrating that K3 and vIF2a had no effect on yeast cell growth (Figure 2A). In contrast, induction of PKR expression was toxic in the vector-transformed yeast, whereas the toxicity was suppressed by co-expression of K3L or vIF2a (Figure 2B). Based on the homology of vIF2a with eIF2a throughout the entire ORF we tested whether suppression of PKR toxicity might be caused by the
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E 6x coverage mammalian genomes were used to build a profile hidden Markov model with the software HMMER [81], which was then used to screen the platypus ab initio peptide predictions available from Ensembl. An inferred ancestral HIN domain sequence from the node that predates the split between HIN-A, -B and -C domains was also used to perform this search. The genomes of chicken (Gallus gallus rel
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The vector pEMBLyex4, were introduced into the temperature-sensitive eIF2a (sui2-1, TD304-10B) mutant strain. The indicated transformants were streaked on SC-Gal medium, where eIF2a expression was maintained and the viral protein expression was induced, and incubated at the indicated temperatures. Results shown are representative of 4 independent transformants for each plasmid.Rothenburg et al. BM