Evidence map›Paper›PMID 8350414›Full record

ArticleJournal of virology1993

Functional analysis of interactions between Tat and the trans-activation response element of human immunodeficiency virus type 1 in cells.

Y Luo, S J Madore, T G Parslow, B R Cullen, B M Peterlin

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 43 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Y LuoHoward Hughes Medical Institute, University of California, San Francisco 94143.
S J Madore
T G Parslow
B R Cullen
B M Peterlin
Howard Hughes Medical Institute · USUniversity of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcriptional trans-activation of the human immunodeficiency virus type 1 long terminal repeat requires that the virally encoded Tat effector interacts with its target trans-activation response element (TAR) RNA stem-loop. Although the arginine-rich region of Tat from amino acids 49 to 59 is sufficient to bind to TAR RNA in vitro, the RNA-binding domain of Tat has not been defined in vivo. Human immunodeficiency virus type 1 also encodes the Rev protein, which acts through an RNA stem-loop called the Rev-response element to transport unspliced and singly spliced viral RNA species from the nucleus to the cytoplasm. To map the RNA-binding domain of Tat, we performed assays that relied on Rev function using the heterologous RNA-tethering mechanism of Tat and the TAR. By examining the effects of selected targeted mutations of Tat on the abilities of hybrid Tat/Rev proteins to rescue the expression of unspliced mRNA via the TAR, we demonstrated that residues throughout the N-terminal 59 amino acids of Tat are required for binding of Tat and TAR RNA in vivo.

Indexed as

HIV Long Terminal RepeatTranscriptional ActivationAnimalsBase SequenceCell LineChloramphenicol O-AcetyltransferaseGene ExpressionGene Products, revGene Products, tatHIV-1Molecular Sequence DataNucleic Acid ConformationPlasmidsProtein BindingRecombinant Proteinsrev Gene Products, Human Immunodeficiency VirusChloramphenicol O-AcetyltransferaseGene Products, revGene Products, tatRecombinant Proteinsrev Gene Products, Human Immunodeficiency VirusRNA, MessengerRNA, Viraltat Gene Products, Human Immunodeficiency Virus

Identifiers

PMID8350414
PMCPMC237965
OpenAlexW1832453117

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.