p38丝裂原活化蛋白激酶（MAPK）和MK2信号通路对于依赖分化的人乳头瘤病毒生命周期至关重要。
p38MAPK and MK2 pathways are important for the differentiation-dependent human papillomavirus life cycle.
作者信息
Satsuka Ayano, Mehta Kavi, Laimins Laimonis
机构信息
Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA
出版信息
J Virol. 2015 Feb;89(3):1919-24. doi: 10.1128/JVI.02712-14. Epub 2014 Nov 19.
Abstract
Amplification of human papillomaviruses (HPV) is dependent on the ATM DNA damage pathway. In cells with impaired p53 activity, DNA damage repair requires the activation of p38MAPK along with MAPKAP kinase 2 (MK2). In HPV-positive cells, phosphorylation of p38 and MK2 proteins was induced along with relocalization to the cytoplasm. Treatment with MK2 or p38 inhibitors blocked HPV genome amplification, identifying the p38/MK2 pathway as a key regulator of the HPV life cycle.
摘要
人乳头瘤病毒（HPV）的扩增依赖于ATM DNA损伤途径。在p53活性受损的细胞中，DNA损伤修复需要p38丝裂原活化蛋白激酶（p38MAPK）以及丝裂原活化蛋白激酶相关激酶2（MK2）的激活。在HPV阳性细胞中，p38和MK2蛋白的磷酸化伴随着重新定位到细胞质中而被诱导。用MK2或p38抑制剂处理可阻断HPV基因组扩增，确定p38/MK2途径是HPV生命周期的关键调节因子。
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