Evidence map›Paper›PMID 11507194›Full record

ArticleJournal of virology2001

RNA splicing at human immunodeficiency virus type 1 3' splice site A2 is regulated by binding of hnRNP A/B proteins to an exonic splicing silencer element.

P S Bilodeau, J K Domsic, A Mayeda, A R Krainer, C M Stoltzfus

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

54 citing papers in PubMed, 116 citations in OpenAlex.

  1. Review
  2. Helicobacter Pylori-Enhanced hnRNPA2B1 Coordinates with PABPC1 to Promote Non-mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Let It Go: HIV-1Journal of virology · 2021
    Review
  8. Review
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  10. Review
  11. Article
  12. Review
  13. Article
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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 3 institutions in 1 country.

P S BilodeauDepartment of Microbiology, University of Iowa, Iowa City, Iowa 52242, USA.
J K Domsic
A Mayeda
A R Krainer
C M Stoltzfus
University of Iowa · USCold Spring Harbor Laboratory · USUniversity of Miami · US

Funding

VIRAL TRANSACTIVATIONP01CA013106 · NCI · COLD SPRING HARBOR LABORATORY · PI William Richard McCombie · 1985 to 2026
$116.8M
REGULATION OF HIV-1 RNA SPLICINGR01AI036073 · NIAID · UNIVERSITY OF IOWA · PI AMENDT, BRAD · 1995 to 2010
$2.5M
Regulation of HIV-1 RNA SplicingR56AI036073 · NIAID · UNIVERSITY OF IOWA · PI STOLTZFUS, CONRAD · 2005 to 2005
$332k
NCI NIH HHS CA13106NCI NIH HHS P01 CA013106NIAID NIH HHS AI36073NIAID NIH HHS R01 AI036073NIAID NIH HHS R56 AI036073
6 · The paper itself

Abstract

The synthesis of human immunodeficiency virus type 1 (HIV-1) mRNAs is a complex process by which more than 30 different mRNA species are produced by alternative splicing of a single primary RNA transcript. HIV-1 splice sites are used with significantly different efficiencies, resulting in different levels of mRNA species in infected cells. Splicing of Tat mRNA, which is present at relatively low levels in infected cells, is repressed by the presence of exonic splicing silencers (ESS) within the two tat coding exons (ESS2 and ESS3). These ESS elements contain the consensus sequence PyUAG. Here we show that the efficiency of splicing at 3' splice site A2, which is used to generate Vpr mRNA, is also regulated by the presence of an ESS (ESSV), which has sequence homology to ESS2 and ESS3. Mutagenesis of the three PyUAG motifs within ESSV increases splicing at splice site A2, resulting in increased Vpr mRNA levels and reduced skipping of the noncoding exon flanked by A2 and D3. The increase in Vpr mRNA levels and the reduced skipping also occur when splice site D3 is mutated toward the consensus sequence. By in vitro splicing assays, we show that ESSV represses splicing when placed downstream of a heterologous splice site. A1, A1(B), A2, and B1 hnRNPs preferentially bind to ESSV RNA compared to ESSV mutant RNA. Each of these proteins, when added back to HeLa cell nuclear extracts depleted of ESSV-binding factors, is able to restore splicing repression. The results suggest that coordinate repression of HIV-1 RNA splicing is mediated by members of the hnRNP A/B protein family.

Indexed as

3' Untranslated RegionsExonsGene SilencingHeterogeneous-Nuclear Ribonucleoprotein Group A-BRNA SplicingRNA, Viral5' Untranslated RegionsBinding SitesConsensus SequenceHeLa CellsHeterogeneous Nuclear Ribonucleoprotein A1Heterogeneous-Nuclear RibonucleoproteinsHIV-1HumansMutagenesisRibonucleoproteins3' Untranslated Regions5' Untranslated RegionsHeterogeneous Nuclear Ribonucleoprotein A1Heterogeneous-Nuclear Ribonucleoprotein Group A-BHeterogeneous-Nuclear RibonucleoproteinshnRNP A2RibonucleoproteinsRNA, Viral

Identifiers

PMID11507194
PMCPMC115094
OpenAlexW2117052867

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.