Evidence map›Paper›PMID 31665504›Full record

ArticleNucleic acids research2019

A dynamic i-motif with a duplex stem-loop in the long terminal repeat promoter of the HIV-1 proviral genome modulates viral transcription.

Emanuela Ruggiero, Sara Lago, Primož Šket, Matteo Nadai, Ilaria Frasson, Janez Plavec, Sara N Richter

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 50 citations in OpenAlex.

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  17. Structure of i-Motif/Duplex Junctions at Neutral pH.Journal of the American Chemical Society · 2021
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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

7 authors at 2 institutions in 2 countries.

Emanuela RuggieroDepartment of Molecular Medicine, University of Padua, 35121 Padua, Italy.
Sara LagoDepartment of Molecular Medicine, University of Padua, 35121 Padua, Italy.
Primož ŠketSlovenian NMR center, National Institute of Chemistry, Hajdrihova, 19, Ljubljana SI-1000, Slovenia.
Matteo NadaiDepartment of Molecular Medicine, University of Padua, 35121 Padua, Italy.
Ilaria FrassonDepartment of Molecular Medicine, University of Padua, 35121 Padua, Italy.
Janez PlavecSlovenian NMR center, National Institute of Chemistry, Hajdrihova, 19, Ljubljana SI-1000, Slovenia.
Sara N RichterDepartment of Molecular Medicine, University of Padua, 35121 Padua, Italy.
University of Padua · ITNational Institute of Chemistry · SI

Funding

European Research Council 615879
6 · The paper itself

Abstract

I-motifs are non-canonical nucleic acids structures characterized by intercalated H-bonds between hemi-protonated cytosines. Evidence on the involvement of i-motif structures in the regulation of cellular processes in human cells has been consistently growing in the recent years. However, i-motifs within non-human genomes have never been investigated. Here, we report the characterization of i-motifs within the long terminal repeat (LTR) promoter of the HIV-1 proviral genome. Biophysical and biochemical analysis revealed formation of a predominant i-motif with an unprecedented loop composition. One-dimensional nuclear magnetic resonance investigation demonstrated formation of three G-C H-bonds in the long loop, which likely improve the structure overall stability. Pull-down experiments combined with mass spectrometry and protein crosslinking analysis showed that the LTR i-motif is recognized by the cellular protein hnRNP K, which induced folding at physiological conditions. In addition, hnRNP K silencing resulted in an increased LTR promoter activity, confirming the ability of the protein to stabilize the i-motif-forming sequence, which in turn regulates the LTR-mediated HIV-1 transcription. These findings provide new insights into the complexity of the HIV-1 virus and lay the basis for innovative antiviral drug design, based on the possibility to selectively recognize and target the HIV-1 LTR i-motif.

Indexed as

HIV-1HIV Long Terminal RepeatPromoter Regions, GeneticProvirusesBinding SitesGene Expression Regulation, ViralHeterogeneous-Nuclear Ribonucleoprotein KRNA, ViralTranscription, GeneticVirus ReplicationHeterogeneous-Nuclear Ribonucleoprotein KRNA, Viral

Identifiers

PMID31665504
PMCPMC6868428
OpenAlexW2982374301

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LicenceCC BY
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Registered trials

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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.