Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2008-9-29
pubmed:abstractText
Apolipoprotein B mRNA-editing enzyme catalytic polypeptide 3 protein G (APOBEC3G) is part of the innate immune system of host cells and has cytidine deaminase activity. It specifically incorporates into the virion during HIV-1 replication. The incorporation of APOBEC3G needs its interaction with HIV-1 Gag. In the HIV-1 reverse transcription process, APOBEC3G deaminates dC to dU in the first minus strand cDNA, and then induces extensive hypermutation in the viral genome. Besides deamination, APOBEC3G also inhibits HIV-1 by some kinds of non-deamination mechanisms which need to be further elucidated. HIV-1 Vif counteracts the activity of APOBEC3G by an ubiquitin-proteasome-mediated degradation of APOBEC3G. As a broad spectrum inhibitor of viruses, APOBEC3G also inhibits various retroviruses, retrotransposons and other viruses like HBV. Upregulating the expression of APOBEC3G or blocking the Vif-mediated degradation of APOBEC3G might be novel strategies to treat HIV-1 infection in the future.
pubmed:grant
pubmed:language
chi
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0513-4870
pubmed:author
pubmed:issnType
Print
pubmed:volume
43
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
678-82
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
[Advances in the study of molecular mechanism of APOBEC3G anti-HIV-1].
pubmed:affiliation
Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
pubmed:publicationType
Journal Article, English Abstract, Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural