Trafficking of UL37 Proteins into Mitochondrion-Associated Membranes during Permissive Human Cytomegalovirus Infection

被引:32
作者
Bozidis, Petros [1 ]
Williamson, Chad D. [1 ,2 ]
Wong, Daniel S. [1 ]
Colberg-Poley, Anamaris M. [1 ,2 ,3 ]
机构
[1] Childrens Natl Med Ctr, Ctr Canc & Immunol Res, Childrens Res Inst, Washington, DC 20010 USA
[2] George Washington Univ, Dept Biochem & Mol Biol, Washington, DC 20037 USA
[3] George Washington Univ, Sch Med & Hlth Sci, Dept Pediat, Washington, DC 20037 USA
关键词
ENDOPLASMIC-RETICULUM; LOCALIZED INHIBITOR; INDUCED APOPTOSIS; CYTOCHROME B(5); GENE-EXPRESSION; CALCIUM; VMIA; BAX; GLYCOPROTEIN; SIGNAL;
D O I
10.1128/JVI.00885-10
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Human cytomegalovirus (HCMV) UL37 proteins traffic sequentially from the endoplasmic reticulum (ER) to the mitochondria. In transiently transfected cells, UL37 proteins traffic into the mitochondrion-associated membranes (MAM), the site of contact between the ER and mitochondria. In HCMV-infected cells, the predominant UL37 exon 1 protein, pUL37x1, trafficked into the ER, the MAM, and the mitochondria. Surprisingly, a component of the MAM calcium signaling junction complex, cytosolic Grp75, was increasingly enriched in heavy MAM from HCMV-infected cells. These studies show the first documented case of a herpesvirus protein, HCMV pUL37x1, trafficking into the MAM during permissive infection and HCMV-induced alteration of the MAM protein composition.
引用
收藏
页码:7898 / 7903
页数:6
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