Source:http://linkedlifedata.com/resource/entrezgene/interaction/8065-155459
| Predicate | Object |
|---|---|
| rdf:type | |
| entrezgene:pubmed |
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pubmed-article:22479405
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| entrezgene:interactant | |
| entrezgene:geneRifText |
Affinity Capture-MS; Affinity Capture-Western; Co-purification; Reconstituted Complex,
CUL5/RBX2/ELOB/ELOC/Vif/CBF-beta complex catalyzes polyubiquitin chain formation on A3G in the presence of ubiquitin E2 UBE2R1 (CDC34) or UBCH5b (UBE2D2),
Chim3, corresponding to amino acids 126-170 of the natural mutant F12-Vif, interacts poorly with Cul5 but affects HIV-1 Vif/Cul5 interaction,
Deletion of amino acids 120 to 138 in Cul5 significantly reduces its interaction with HIV-1 Vif, but does not affect Cul5 binding to Elongins B/C; the HCCH zinc-binding motif (residues 108-139) in Vif is required for the interaction with Cul5,
HIV-1 Vif (amino acids 144-149; SLQXLA motif; BC-box) interacts with cellular proteins Cul5, elongins B and C, and Rbx1 to form an Skp1-Cullin-F-box (SCF)-like complex that allows Vif to interact with APOBEC3G and induce its ubiquitination and degradation,
HIV-1 Vif YF111/112AA, F115A, I120S and AL123/124SS mutants are unable to recruit Cul5, but retain interactions with Elongin B and C proteins,
HIV-1 Vif is regulated by Cullin5 E3 ligase and its expression levels increases in the presence of a Cullin5 dominant negative mutant, Cul5deltaNedd8,
HIV-1 Vif ubiquitination is promoted by Cul5 in vitro and in vivo in a manner that requires an intact SOCS-box motif in Vif, and auto ubiquitination of Vif occurs within an assembled Vif-Cul5 complex,
HIV-1 Vif, CBF-beta, CUL5, and ELOB/C form a complex that is required for Vif-mediated downregulation of A3G and A3F. CBF-beta regulates HIV-1 infectivity only in the presence of A3G,
HIV-1 Vif-induced G2 accumulation requires a Cul5-based E3 ligase, but is independent of APOBEC3D/E, F, and G expression. Overexpression of ubiquitin(K48R) abolishes Vif-induced G2 accumulation,
Mutations in HIV-1 Vif PPLP motif (amino acids 161-164) reduces Vif binding to A3G without affecting its interaction with ElonginC and Cullin5,
The T(Q/D/E)x(5)ADx(2)(I/L) motif, located at residues 96 to 107 in HIV-1 Vif, regulates Vif interaction with Cul5,
The amino acids L163 and L169 located downstream of the SOCS-box motif in HIV-1 Vif are required for Vif function and efficient interaction with Cul5-ElonginB-ElonginC,
Treatment with the membrane-permeable zinc chelator TPEN prevents Vif function, and causes the blockage of Cul5 recruitment and APOBEC3G (A3G) degradation,
Two highly conserved Cys residues (C114 and C133) outside the SOCS box (amino acids 144-169) motif in HIV-1 Vif are required for the interaction of Vif with Cul5 but not ElonginC,
Vif-induced ubiquitination of A3G and A3G20K/R is inhibited by Cul5deltaNedd8
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| entrezgene:interactionSourc... |
BioGRID
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| entrezgene:keyphrase |
interacts with,
inhibited by,
regulated by,
requires,
complexes with
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