Linked Life Data

17896967

Source:http://linkedlifedata.com/resource/pubmed/id/17896967

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2007-9-27
pubmed:abstractText
The role of Tat in HIV-1 reverse transcription has been controversial largely because different studies have observed disparate effects of the Tat protein on reverse transcription. Studies of HIV-1 lacking a functional tat gene demonstrated a decrease in reverse transcription efficiency following infection of T-cells however, in vitro recombinant Tat(1-86) has been shown to inhibit RT activity. Here we show that 20-200 nM of both N-terminally histidine-tagged recombinant Tat(1-72) and Tat(1-86) stimulated reverse transcription by HIV-1 reverse transcriptase (RT) in vitro by 2-3 fold. However, both Tat species were efficient inhibitors of RT activity at 400 nM. The lower concentrations of Tat increased reverse transcription efficiency by facilitating multiple rounds of DNA synthesis, and this increase was either not seen or reduced when Tat proteins with multiply-mutated cysteine or basic domains were used. Tat-enhanced reverse transcription occurred in a RNA-independent manner, and required formation of a Tat-RT complex. Pull-down and immunoprecipitation experiments confirmed that Tat could interact with the RT p51 subunit, and mammalian two-hybrid experiments showed interaction between Tat and both the p51 and p66 subunits. Together these results provide evidence that Tat can stimulate reverse transcription through an interaction with RT.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1873-4251
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
473-83
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
The HIV-1 Tat protein stimulates reverse transcription in vitro.
pubmed:affiliation
Division of Immunology and Infectious Disease, Queensland Institute of Medical Research, Brisbane, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't