T-cell differentiation factor CBF- b regulates HIV-1 Vif-mediated evasion of host restriction英文学习资料.PDFVIP

LETTER doi:10.1038/nature10718 T-cell differentiation factor CBF-b regulates HIV-1 Vif-mediated evasion of host restriction 1 1,2 2 2 1,2 Wenyan Zhang *, Juan Du *, Sean L. Evans , Yunkai Yu Xiao-Fang Yu The human APOBEC3 cytidine deaminases are potent inhibitors interaction between HIV-1 Vif–HA and CBF-b in transfected 293T of diverse retroviruses, including human immunodeficiency virus-1 (human embryonic kidney) cells (Fig. 1c, lane 4), indicating that the (HIV-1)1–6. HIV-1 Vif forms an E3 ubiquitin ligase complex with interaction between CBF-b and HIV-1 Vif can occur in the absence of cullin 5 (CUL5), elongin B and elongin C 7–9, which promotes the + + + – – – siRNA control polyubiquitination and degradation of APOBEC3 substrates7,10–14. a d – – – + + + CBF-β siRNA Here we demonstrate in human T cells that core binding factor b CUL5 90 + + + + + + A3G–HA – + – – + – NL4-3ΔVif (CBF-b) is a key regulator of the evasion of HIV-1 from the host – – + – – + NL4-3 defence mediated by APOBEC3. CBF-b, the non-DNA-binding 50 Pr55Gag subunit of a heterodimeric transcription factor, regulates the folding