ArticleRetrovirology2008
Refined study of the interaction between HIV-1 p6 late domain and ALIX.
Article in Retrovirology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- HIV Genome-Wide Protein Associations: a Review of 30 Years of Research.Microbiology and molecular biology reviews : MMBR · 2016Pooled it
- PYRE insertion within HIV-1 subtype C p6-Gag functions as an ALIX-dependent late domain.Scientific reports · 2018Article
- ALIX Rescues Budding of a Double PTAP/PPEY L-Domain Deletion Mutant of Ebola VP40: A Role for ALIX in Ebola Virus Egress.The Journal of infectious diseases · 2015Article
- The phosphorylation of HIV-1 Gag by atypical protein kinase C facilitates viral infectivity by promoting Vpr incorporation into virions.Retrovirology · 2014Article
- The S40 residue in HIV-1 Gag p6 impacts local and distal budding determinants, revealing additional late domain activities.Retrovirology · 2013Article
- Sprouty 2 binds ESCRT-II factor Eap20 and facilitates HIV-1 gag release.Journal of virology · 2011Article
- Highly conserved serine residue 40 in HIV-1 p6 regulates capsid processing and virus core assembly.Retrovirology · 2011Article
- Transmission of new CRF07_BC strains with 7 amino acid deletion in Gag p6.Virology journal · 2011Article
- An LYPSL late domain in the gag protein contributes to the efficient release and replication of Rous sarcoma virus.Journal of virology · 2010Article
- A crescent-shaped ALIX dimer targets ESCRT-III CHMP4 filaments.Structure (London, England : 1993) · 2009Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The interaction between the HIV-1 p6 late budding domain and ALIX, a class E vacuolar protein sorting factor, was explored by using the yeast two-hybrid approach. We refined the ALIX binding site of p6 as being the leucine triplet repeat sequence (Lxx)4 (LYPLTSLRSLFG). Intriguingly, the deletion of the C-terminal proline-rich region of ALIX prevented detectable binding to p6. In contrast, a four-amino acid deletion in the central hinge region of p6 increased its association with ALIX as shown by its ability to bind to ALIX lacking the proline rich domain. Finally, by using a random screening approach, the minimal ALIX391-510 fragment was found to specifically interact with this p6 deletion mutant. A parallel analysis of ALIX binding to the late domain p9 from EIAV revealed that p6 and p9, which exhibit distinct ALIX binding motives, likely bind differently to ALIX. Altogether, our data support a model where the C-terminal proline-rich domain of ALIX allows the access of its binding site to p6 by alleviating a conformational constraint resulting from the presence of the central p6 hinge.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.