Induction of Ubiquitination and Degradation of APOBEC3G by HIV-1 Vif-Cul5-SCF
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منابع مشابه
Induction of APOBEC3G ubiquitination and degradation by an HIV-1 Vif-Cul5-SCF complex.
Human immunodeficiency virus-1 (HIV-1) Vif is essential for viral evasion of host antiviral factor CEM15/APOBEC3G. We report that Vif interacts with cellular proteins Cul5, elongins B and C, and Rbx1 to form an Skp1-cullin-F-box (SCF)-like complex. The ability of Vif to suppress antiviral activity of APOBEC3G was specifically dependent on Cul5-SCF function, allowing Vif to interact with APOBEC3...
متن کاملPhosphorylation of a novel SOCS-box regulates assembly of the HIV-1 Vif-Cul5 complex that promotes APOBEC3G degradation.
HIV-1 Vif (viral infectivity factor) protein overcomes the antiviral activity of the DNA deaminase APOBEC3G by targeting it for proteasomal degradation. We report here that Vif targets APOBEC3G for degradation by forming an SCF-like E3 ubiquitin ligase containing Cullin 5 and Elongins B and C (Cul5-EloB-EloC) through a novel SOCS (suppressor of cytokine signaling)-box that binds EloC. Vif bindi...
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Human immunodeficiency virus-1 (HIV-1) Vif overcomes the anti-viral activity of APOBEC3G by targeting it for ubiquitination via a Cullin 5-ElonginB-ElonginC (Cul5-EloBC) E3 ligase. Vif associates with Cul5-EloBC through a BC-box motif that binds EloC, but the mechanism by which Vif selectively recruits Cul5 is poorly understood. Here we report that a region of Vif (residues 100-142) upstream of...
متن کاملAssociations between HIV Susceptibility and Mutations in the Vif-associated APOBEC3G Proteasomal Complex
The purpose of this experiment was to determine whether a host’s single nucleotide polymorphisms (SNPs) in the Vifassociated APOBEC3G Proteasomal Complex influence his/her innate immunity to Human Immunodeficiency Virus-1. The experimenters compared host DNA at specific sites on each patient’s genome (SNPs) and the patient’s HIV1 disease progression. They extracted DNA from peripheral blood mon...
متن کاملVif hijacks CBF-b to degrade APOBEC3G and promote HIV-1 infection
Restriction factors, such as the retroviral complementary DNA deaminase APOBEC3G, are cellular proteins that dominantly block virus replication. TheAIDSvirus, human immunodeficiency virus type 1 (HIV-1), produces the accessory factor Vif, which counteracts the host’s antiviral defence by hijacking a ubiquitin ligase complex, containing CUL5, ELOC, ELOB and a RING-box protein, and targeting APOB...
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تاریخ انتشار 2003