Please use this identifier to cite or link to this item:
https://hdl.handle.net/10316/107185
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Ali, Hashim | - |
dc.contributor.author | Mano, Miguel | - |
dc.contributor.author | Braga, Luca | - |
dc.contributor.author | Naseem, Asma | - |
dc.contributor.author | Marini, Bruna | - |
dc.contributor.author | Vu, Diem My | - |
dc.contributor.author | Collesi, Chiara | - |
dc.contributor.author | Meroni, Germana | - |
dc.contributor.author | Lusic, Marina | - |
dc.contributor.author | Giacca, Mauro | - |
dc.date.accessioned | 2023-06-13T11:10:11Z | - |
dc.date.available | 2023-06-13T11:10:11Z | - |
dc.date.issued | 2019-02-25 | - |
dc.identifier.issn | 2041-1723 | pt |
dc.identifier.uri | https://hdl.handle.net/10316/107185 | - |
dc.description.abstract | Productive HIV-1 replication requires viral integrase (IN), which catalyzes integration of the viral genome into the host cell DNA. IN, however, is short lived and is rapidly degraded by the host ubiquitin-proteasome system. To identify the cellular factors responsible for HIV-1 IN degradation, we performed a targeted RNAi screen using a library of siRNAs against all components of the ubiquitin-conjugation machinery using high-content microscopy. Here we report that the E3 RING ligase TRIM33 is a major determinant of HIV-1 IN stability. CD4-positive cells with TRIM33 knock down show increased HIV-1 replication and proviral DNA formation, while those overexpressing the factor display opposite effects. Knock down of TRIM33 reverts the phenotype of an HIV-1 molecular clone carrying substitution of IN serine 57 to alanine, a mutation known to impair viral DNA integration. Thus, TRIM33 acts as a cellular factor restricting HIV-1 infection by preventing provirus formation. | pt |
dc.language.iso | eng | pt |
dc.publisher | Springer Nature | pt |
dc.relation | Intramural Funding Programme of the ICGEB to the Molecular Medicine Laboratory in Trieste, Italy | pt |
dc.rights | openAccess | pt |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | pt |
dc.subject.mesh | HIV Infections | pt |
dc.subject.mesh | HIV Integrase | pt |
dc.subject.mesh | HIV-1 | pt |
dc.subject.mesh | Host-Pathogen Interactions | pt |
dc.subject.mesh | Humans | pt |
dc.subject.mesh | Proteasome Endopeptidase Complex | pt |
dc.subject.mesh | Protein Stability | pt |
dc.subject.mesh | Proteolysis | pt |
dc.subject.mesh | Proviruses | pt |
dc.subject.mesh | Transcription Factors | pt |
dc.subject.mesh | Virus Integration | pt |
dc.title | Cellular TRIM33 restrains HIV-1 infection by targeting viral integrase for proteasomal degradation | pt |
dc.type | article | - |
degois.publication.firstPage | 926 | pt |
degois.publication.issue | 1 | pt |
degois.publication.title | Nature Communications | pt |
dc.peerreviewed | yes | pt |
dc.identifier.doi | 10.1038/s41467-019-08810-0 | pt |
degois.publication.volume | 10 | pt |
dc.date.embargo | 2019-02-25 | * |
uc.date.periodoEmbargo | 0 | pt |
item.languageiso639-1 | en | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.grantfulltext | open | - |
item.fulltext | Com Texto completo | - |
item.cerifentitytype | Publications | - |
item.openairetype | article | - |
crisitem.author.researchunit | CNC - Center for Neuroscience and Cell Biology | - |
crisitem.author.orcid | 0000-0003-1922-4824 | - |
Appears in Collections: | I&D CNC - Artigos em Revistas Internacionais |
Files in This Item:
File | Description | Size | Format | |
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Cellular-TRIM33-restrains-HIV1-infection-by-targeting-viral-integrase-for-proteasomal-degradationNature-Communications.pdf | 2.79 MB | Adobe PDF | View/Open |
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