@article{oai:nagasaki-u.repo.nii.ac.jp:00001338,
 author = {Kamiyama, Haruka and Izumida, Mai and Umemura, Yuria and Hayashi, Hideki and Matsuyama, Toshifumi and Kubo, Yoshinao},
 journal = {Frontiers in Microbiology},
 month = {Aug},
 note = {Host-cell expression of the ezrin protein is required for CXCR4 (X4)-tropic HIV-1 infection. Ezrin function is regulated by phosphorylation at threonine-567. This study investigates the role of ezrin phosphorylation in HIV-1 infection and virion release. We analyzed the effects of ezrin mutations involving substitution of threonine-567 by alanine (EZ-TA), a constitutively inactive mutant, or by 
aspartic acid (EZ-TD), which mimics phosphorylated threonine. We also investigated the effects of ezrin silencing on HIV-1 virion release using a specific siRNA. We observed that X4-tropic HIV-1 
vector infection was inhibited by expression of the EZ-TA mutant but increased by expression of the EZ-TD mutant, suggesting that ezrin phosphorylation in target cells is required for efficient HIV-1 entry. Expression of a dominant-negative mutant of ezrin (EZ-N) and ezrin silencing in HIV-1 vector-producing cells significantly reduced the infectivity of released virions without affecting virion production. This result indicates that endogenous ezrin expression is required for virion infectivity. The EZ-TD but not the EZ-TA inhibited virion release from HIV-1 vector-producing cells. 
Taken together, these findings suggest that ezrin phosphorylation in target cells is required for efficient HIV-1 entry but inhibits virion release from HIV-1 vector-producing cells., Frontiers in Microbiology, 9, art.no.1912; 2018},
 title = {Role of Ezrin Phosphorylation in HIV-1 Replication},
 volume = {9},
 year = {2018}
}