FEATURES

FAMILY

DESCRIPTION

Also known as VPR_SIVEK, vpr. During virus replication, may deplete host UNG protein, and incude G2-M cell cycle arrest. Acts by targeting specific host proteins for degradation by the 26S proteasome, through association with the cellular CUL4A-DDB1 E3 ligase complex by direct interaction with host VPRPB/DCAF-1. Cell cycle arrest reportedly occurs within hours of infection and is not blocked by antiviral agents, suggesting that it is initiated by the VPR carried into the virion. Additionally, VPR induces apoptosis in a cell cycle dependent manner suggesting that these two effects are mechanistically linked. Detected in the serum and cerebrospinal fluid of AIDS patient, VPR may also induce cell death to bystander cells., During virus entry, plays a role in the transport of the viral pre-integration (PIC) complex to the host nucleus. This function is crucial for viral infection of non-dividing macrophages. May act directly at the nuclear pore complex, by binding nucleoporins phenylalanine-glycine (FG)-repeat regions. Homooligomer, may form homodimer. Interacts with p6-gag region of the Pr55 Gag precursor protein through a (Leu-X-X)4 motif near the C-terminus of the P6gag protein. Interacts with host UNG. May interact with host RAD23A/HHR23A. Interacts with host VPRBP/DCAF1, leading to hijack the CUL4A-RBX1-DDB1-DCAF1/VPRBP complex, mediating ubiquitination of host proteins such as TERT and ZGPAT and arrest of the cell cycle in G2 phase.

vpr

Structural Ligandability

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Distribution