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来源:百度知道 编辑:UC知道 时间:2024/06/02 05:52:40
Evidence of an IFN response in Pr4△35-infected macrophages
was supported by data indicating a possible role for the
protein kinase PKR in the mutant phenotype. PKR is an IFNinduced
serine-threonine protein kinase with potent antiviral
activity (9). PKR becomes autophosphorylated and activated
in response to dsRNA (9). Although PKR was not represented
in our swine microarray, differential expression of p58 and
PACT, two genes involved in regulating PKR activity, suggested
involvement of PKR in the response to Pr4△35 infection.
p58, a member of the tetratricopeptide repeat family of
proteins and a cellular inhibitor of PKR that is activated in
response to viral infection, was up-regulated in both Pr4- and
Pr4△35-infected cells in comparison to mock-infected cells
(Table 1) (29). In Pr4△35, up-regulation of p58 was not as
pronounced and RNA expression levels were twofold lower
than in Pr4 (0.456 [range, 0.277 to 0.

证据的干扰素反应pr4△35 -巨噬细胞感染获得的数据表明了可能发挥作用的蛋白激酶 pkr的突变7.40% . pkr是ifninduced丝氨酸苏氨酸蛋白激酶服用抗病毒药物( 9 ) . pkr成为autophosphorylated并启动响应dsrna ( 9 ) . 虽然pkr不代表我们猪芯片,差异表达p58和条约 两个基因参与调节pkr活动,建议参与pkr在回应pr4△35感染. p58 , 成员之一tetratricopeptide重复序列家族的蛋白质和细胞抑制剂pkr即启动反应 为病毒感染,上调两个pr4和pr4△35感染细胞相较于模拟感染细胞(表1 ) ( 29 ) . 在pr4△35 上调p58并不象看上去和RNA表达水平的两倍低于pr4 ( 0.456 [范围 0.277至0.698〕; t检验P = 4.27 * 10的-6次方) . 该条约基因(激活pkr )表示,在更高层次pr4△35 -比pr4感染的细胞(见表1 ) . 较低的毒性,提高了条约pr4△35显示pkr抗病毒作用可能存在 在pr4△35感染.