Human Interaction Network Ontology

Last uploaded: June 27, 2014
Jump to:
Id http://purl.obolibrary.org/obo/HINO_0015681
http://purl.obolibrary.org/obo/HINO_0015681
Preferred Name

Vif-mediated degradation of APOBEC3G
Definitions
The HIV-1 accessory protein Vif (Viral infectivity factor) is required for the efficient infection of primary cell populations (e.g., lymphocytes and macrophages) and “non-permissive” cell lines. Vif neutralises the host DNA editing enzyme, APOBEC3G, in the producer cell. Indeed, in the absence of a functional Vif, APOBEC3G is selectively incorporated into the budding virions and in the next cycle of infection leads to the deamination of deoxycytidines (dC) within the minus-strand cDNA during reverse transcription (Sheehy et al 2003; Li et al., 2005 ; Stopak et al. 2003).<br>Deamination changes cytidine to uracil and thus results in G to A transitions and stop codons in the provirus. The aberrant cDNAs produced in the infected cell can either be integrated in form of non-functional proviruses or degraded. Vif counteracts the antiviral activity of APOBEC3G by associating directly with it and promoting its polyubiquitination and degradation by the 26S proteasome. <br>Vif binds APOBEC3G and recruits it into an E3 ubiquitin-enzyme complex composed by the cytoplasmic proteins Cullin5, Rbx, ElonginC and ElonginB (Yu et al., 2003) . Thus, in the presence of Vif, APOBEC3G incorporation into the virion is minimal.<br> Edited: Matthews, L, 2007-01-30 11:27:41 Reviewed: Mulder, L, 2007-01-30 22:57:00 Reviewed: Simon, V, 2007-01-30 23:07:12 Authored: Matthews, L, 2006-05-15 23:53:25
Type http://www.w3.org/2002/07/owl#Class

All Properties

label
Vif-mediated degradation of APOBEC3G
comment
The HIV-1 accessory protein Vif (Viral infectivity factor) is required for the efficient infection of primary cell populations (e.g., lymphocytes and macrophages) and “non-permissive” cell lines. Vif neutralises the host DNA editing enzyme, APOBEC3G, in the producer cell. Indeed, in the absence of a functional Vif, APOBEC3G is selectively incorporated into the budding virions and in the next cycle of infection leads to the deamination of deoxycytidines (dC) within the minus-strand cDNA during reverse transcription (Sheehy et al 2003; Li et al., 2005 ; Stopak et al. 2003).<br>Deamination changes cytidine to uracil and thus results in G to A transitions and stop codons in the provirus. The aberrant cDNAs produced in the infected cell can either be integrated in form of non-functional proviruses or degraded. Vif counteracts the antiviral activity of APOBEC3G by associating directly with it and promoting its polyubiquitination and degradation by the 26S proteasome. <br>Vif binds APOBEC3G and recruits it into an E3 ubiquitin-enzyme complex composed by the cytoplasmic proteins Cullin5, Rbx, ElonginC and ElonginB (Yu et al., 2003) . Thus, in the presence of Vif, APOBEC3G incorporation into the virion is minimal.<br>
Edited: Matthews, L, 2007-01-30 11:27:41
Reviewed: Mulder, L, 2007-01-30 22:57:00
Reviewed: Simon, V, 2007-01-30 23:07:12
Authored: Matthews, L, 2006-05-15 23:53:25
prefLabel
Vif-mediated degradation of APOBEC3G
located_in
definition source
Reactome, http://www.reactome.org
Pubmed14527406
Pubmed14528300
Pubmed14564014
Pubmed16354571
Pubmed15781449
Pubmed12167863
See more
See less
prefixIRI
HINO:0015681
seeAlso
Reactome Database ID Release 43180585
ReactomeREACT_9453
subClassOf
type
has_part
Add comment
Add proposal
Delete Subject Author Type Created
No notes to display