Alphaherpesviral US3 Kinase Induces Cofilin Dephosphorylation To Reorganize the Actin Cytoskeleton
Alphaherpesviral US3 Kinase Induces Cofilin Dephosphorylation To Reorganize the Actin Cytoskeleton
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DOI：
10.1128/jvi.03107-12
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发表时间：
2013-04-01
影响因子：
5.4
通讯作者：
Favoreel, Herman W.
中科院分区：
文献类型：
--
作者：
Jacob, Thary;Van den Broeke, Celine;Favoreel, Herman W.
保守的α疱疹病毒丝氨酸/苏氨酸激酶US 3引起显著的肌动蛋白重排，与增加的病毒传播相关。在这里，我们表明，伪狂犬病病毒（PRV）的US 3导致激活（去磷酸化）的中央肌动蛋白调节cofilin。一种损害US 3激酶活性的突变和I组p21激活的激酶抑制剂IPA-3抑制US 3介导的cofilin激活。此外，磷酸化模拟S3 D cofilin的表达显著抑制了US 3引起细胞突起和细胞变圆的能力。总之，PRV的US 3激酶导致cofilin的活化（去磷酸化），并且cofilin有助于US 3介导的肌动蛋白重排。
The conserved alphaherpesviral serine/threonine kinase US3 causes dramatic actin rearrangements, associated with increased viral spread. Here, we show that US3 of pseudorabies virus (PRV) leads to activation (dephosphorylation) of the central actin regulator cofilin. A mutation that impairs US3 kinase activity and the group I p21-activated kinase inhibitor IPA-3 inhibited US3-mediated cofilin activation. Additionally, expression of phosphomimetic S3D cofilin significantly suppressed the ability of US3 to cause cell projections and cell rounding. In conclusion, the US3 kinase of PRV leads to activation (dephosphorylation) of cofilin, and cofilin contributes to US3-mediated actin rearrangements.