Abstract
Human immunodeficiency virus type 1 (HIV-1) Vif recruits a Cullin 5 ubiquitin ligase that targets APOBEC3 proteins for degradation. Recently, Vif has also been shown to induce cell cycle disturbance in G2. We show that in contrast to the expression of Vpr, the expression of Vif does not preclude cell division, and therefore, Vif causes delay and not arrest in G 2. We also demonstrate that the interaction of Vif with the ubiquitin ligase is required for cell cycle disruption, as was previously shown for HIV-1 Vpr. The presence of APOBEC3 D/E, F, and G had no influence on Vif-induced alteration of the cell cycle. We conclude that cell cycle delay by Vif is a result of ubiquitination and degradation of a cellular protein that is different from the known APOBEC3 family members.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 9265-9272 |
| Number of pages | 8 |
| Journal | Journal of virology |
| Volume | 82 |
| Issue number | 18 |
| DOIs | |
| State | Published - Sep 2008 |
| Externally published | Yes |
Bibliographical note
Funding Information:We thank Dr. Edward J. Hicks for PIWiding hemglobin sarmples, Dr. Walter E. Nan- for introducing us to the principles and practice of gel electrophoresis, Mm. RaweM M o m , Mr. Gary Davis and Mr. Thanas D. Paul for experinentd assistance and instnrcti on, and b.R obert A. Harris, Marion E. Hodes and Robert C. Karn far helpful CQrments. his work was supported by RIS R C M GrMt No. AMl8057, A h t - b A i d fiam the Prmezc ican Heart Association, funds fm the kart F d of Posey County, kdiana, and the Grace M. ShaJalter Txust.
