HPV16 infection of HaCaTs is dependent on β4 integrin, and α6 integrin processing.

HPV16 infection of HaCaTs is dependent on β4 integrin, and α6 integrin processing.
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DOI:
10.1016/j.virol.2013.10.034
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发表时间:
2014-01-20
期刊:
影响因子:
3.7
通讯作者:
Meneses, Patricio I.
Meneses, Patricio I.
中科院分区:
医学3区
文献类型:
--
作者:
Aksoy, Pinar;Abban, Cynthia Y.;Kiyashka, Elizabeth;Qiang, Weitao;Meneses, Patricio I.

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我们对人乳头瘤病毒(HPV)的认识仍在不断发展。为了进一步研究该领域,我们的实验室专注于确定整合素在病毒内吞进入HaCaT细胞初始步骤中的作用。我们以及其他研究人员先前的发现表明,α6对感染是必需的。在此我们表明α3和β1并非必需,并且我们确定整合素α6β4复合物对HaCaT细胞的感染是必需的。β4的敲低导致HPV16假病毒(PsV)感染显著减少,并且可能最为重要的是导致翻译后α6加工缺陷。我们表明未加工的α6不会定位到细胞表面。我们提出α6β4复合物对于形成内吞复合物是必需的,而该内吞复合物会引发初始内吞所需的信号转导事件。
Our understanding of human papillomavirus (HPV) is still evolving. To further study the field, our laboratory has focused on determining the role of integrins in the initial steps of viral endocytosis into HaCaT cells. Our and others' previous findings have shown that α6 is necessary for infection. Here we show that α3 and β1 were dispensable, and we identified integrin α6β4 complex as necessary for infection in HaCaTs. β4 knock down resulted in a significant decrease in HPV16 PsV infection and perhaps most importantly resulted in defective post-translational α6 processing. We showed that the unprocessed α6 does not localize to the cell surface. We propose that the α6β4 complex is necessary for the formation of an endocytic complex that results in the signaling transduction events necessary for initial endocytosis.
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