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References from Manipulation of the cell cycle by HIV-1. Local targets link to admitted publications; unresolved targets remain external evidence.
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Human immunodeficiency virus type 1 Nef binds to tumor suppressor p53 and protects cells against p53-mediated apoptosis
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Cell cycle arrest by Vpr in HIV-1 virions and insensitivity to antiretroviral agents
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Functional and structural characterization of synthetic HIV-1 Vpr that transduces cells, localizes to the nucleus, and induces G2 cell cycle arrest
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Human immunodeficiency virus type 1 Vpr protein is incorporated into the virion in significantly smaller amounts than gag and is phosphorylated in infected cells
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HIV-1 Gag recruits oligomeric Vpr via two binding sites in p6, but both mature p6 and Vpr are rapidly lost upon target cell entry
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Vpr stimulates viral expression and induces cell killing in human immunodeficiency virus type 1-infected dividing Jurkat T cells
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Human immunodeficiency virus type 1 (HIV-1) Vpr enhances expression from unintegrated HIV-1 DNA
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The SMC5/6 complex compacts and silences unintegrated HIV-1 DNA and is antagonized by Vpr
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Premature activation of the SLX4 complex by Vpr promotes G2/M arrest and escape from innate immune sensing
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HIV-1 Vpr activates the G2 checkpoint through manipulation of the ubiquitin proteasome system
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Human immunodeficiency virus type 1 Vif induces cell cycle delay via recruitment of the same E3 ubiquitin ligase complex that targets APOBEC3 proteins for degradation
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Bimodal expression patterns, and not viral burst sizes, predict the effects of Vpr on HIV-1 proviral populations in jurkat cells
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HIV-1 Vpr drives a tissue residency-like phenotype during selective infection of resting memory T cells
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