Source:http://linkedlifedata.com/resource/entrezgene/interaction/10015-155030
| Predicate | Object |
|---|---|
| rdf:type | |
| entrezgene:pubmed |
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| entrezgene:interactant | |
| entrezgene:geneRifText |
A single amino acid Phe676 of Alix is at the center of a large hydrophobic pocket and is crucial for binding to HIV-1 p6,
AIP1 binds to the LXXLF motif in HIV-1 p6 (amino acids 41-44) and along with TSG101 acts as a component of the viral budding machinery,
AIP1 is incorporated into HIV-1 virions through its interaction with HIV-1 p6,
ALIX proteins with point mutations (Val498Asp, Phe676Asp, and Ile683Asp) that inhibit the p6 36YPLASL41 binding fail to rescue HIV-1 deltaPTAP release or infectivity,
Affinity Capture-Western; Reconstituted Complex,
Alix-mediated rescue of HIV-1 PTAP(-) release requires interaction with Nedd4-1. Ubiquitinated Alix is incorporated into HIV-1 PTAP(-) rescued particles,
An ALIX fragment encompassing residues 391-510 is a minimal p6deltaSQKQ binding site within the middle region of ALIX,
HIV-1 NC-mediated incorporation of ALIX into virions requires the zinc fingers of NC and the Bro1 domain of ALIX,
In the absence of Vpu, Env accumulates extensively within clathrin-coated endosomal structures, including the viral proteins Gag and MA; the tetraspanins CD63 and CD81; the adaptor protein complex AP-3; and AIP1/ALIX, a cellular cofactor for viral budding,
Mutations (Y36A, Y36S/L44H, Y36S/L44R, L41A, and L41R) between p6 residues 36 and 44 inhibit the Alix-p6 interaction,
Natural loss of L35Y36 residues in p6 of HIV-1 subtype C prevents p6 from ALIX interaction,
Overexpression of AIP1(364-716) leads to a reduction in the cell-associated levels of HIV-1 Gag,
Overexpression of AIP1(364-716) severely disrupts Gag processing, resulting in an increase in the ratio of Gag to p25/p24,
Overexpression of the Alix V domain inhibits HIV-1 release from cells; this inhibition of release is reversed by mutations that block binding of the Alix V domain to p6,
Phe105 loop (residues 99-112) in the Bro1 domain of Alix is required for efficient Alix-mediated HIV-1 release. The disruption of the Phe105 loop interferes with its ability to interact with HIV-1 Gag,
Recruitment of CHMP4B by ALIX to HIV-1 Gag puncta is observed in in-vitro membrane model,
Residues 360-702 of Alix spans the shape of the letter 'V' and is termed the V domain, which has a topologically complex arrangement of 11 alpha-helices; Phe676 is at the center of a large hydrophobic pocket and is crucial for binding to HIV-1 p6,
Residues Q8, K11, K48, R51, R56, and K60 are part of the Bro1 domain of ALIX binding to HIV-1 NC, which involves RNA. Disruption of the Bro1-NC binding inhibits ALIX function in virus release,
The Bro1 domain of Alix inhibits HIV budding by targeting both PTAP/TSG101 and LYPXnL/Alix pathways,
The Bro1 domain of Alix inhibits HIV budding by targeting both PTAP/TSG101 and LYPXnL/Alix pathways. The NC domain of Gag is the primary target for Bro1 inhibition by Gag-mediated recruitment of Bro1 to the plasma membrane,
The N-terminal Bro1 domain (Brox) of ALIX bind to HIV-1 NC. Unexpectedly, Brox retains significant activity even if its CHMP4 binding site is disrupted,
The ability of ALIX to rescue an HIV p6 PTAP mutant depends on its C-terminal proline-rich domain (PRD), but not on its binding sites for Tsg101,
The phenolic hydroxyl of the tyrosine residue in the 36YPXnL domain of HIV-1 p6 is essential for ALIX-mediated HIV-1 budding. Y36F mutant blocks ALIX recruitment
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| entrezgene:interactionSourc... |
BioGRID
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| entrezgene:keyphrase |
interacts with,
co-localizes with,
binds,
recruits,
downregulated by,
incorporates,
rescued by
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