Evidence map›Paper›PMID 25293769›Full record

ArticleBlood2014

PARP-14 combines with tristetraprolin in the selective posttranscriptional control of macrophage tissue factor expression.

M Bilal Iqbal, Michael Johns, Jun Cao, Yu Liu, Sheng-Chun Yu, Gareth D Hyde, Michael A Laffan, Francesco P Marchese, Sung Hoon Cho, Andrew R Clark and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.8field-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

41 citing papers in PubMed, 66 citations in OpenAlex.

  1. Review
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  12. IFN-Induced PARPs-Sensors of Foreign Nucleic Acids?Pathogens (Basel, Switzerland) · 2023
    Review
  13. Article
  14. Article
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  16. Functional roles of ADP-ribosylation writers, readers and erasers.Frontiers in cell and developmental biology · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 6 institutions in 2 countries.

M Bilal IqbalVascular Sciences Section, National Heart and Lung Institute, Imperial College London, United Kingdom;
Michael JohnsVascular Sciences Section, National Heart and Lung Institute, Imperial College London, United Kingdom;
Jun CaoVascular Sciences Section, National Heart and Lung Institute, Imperial College London, United Kingdom;
Yu LiuVascular Sciences Section, National Heart and Lung Institute, Imperial College London, United Kingdom;
Sheng-Chun YuVascular Sciences Section, National Heart and Lung Institute, Imperial College London, United Kingdom;
Gareth D HydeVascular Sciences Section, National Heart and Lung Institute, Imperial College London, United Kingdom;
Michael A LaffanDepartment of Medicine, Imperial College London, United Kingdom;
Francesco P MarcheseKennedy Institute of Rheumatology Division, University of Oxford, Oxford, United Kingdom;
Sung Hoon ChoDepartment of Pathology, Microbiology & Immunology, Vanderbilt University, Nashville, TN;
Andrew R ClarkCentre for Translational Inflammation Research, University of Birmingham, Birmingham, United Kingdom;
Felicity N GavinsDepartment of Medicine, Imperial College London, United Kingdom;
Kevin J WoollardDepartment of Medicine, Imperial College London, United Kingdom;
Perry J BlackshearNational Institute of Environmental Health Sciences, Research Triangle Park, NC; and.
Nigel MackmanDepartment of Medicine, McAllister Heart Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC.
Jonathan L DeanKennedy Institute of Rheumatology Division, University of Oxford, Oxford, United Kingdom;
Mark BoothbyDepartment of Pathology, Microbiology & Immunology, Vanderbilt University, Nashville, TN;
Dorian O HaskardVascular Sciences Section, National Heart and Lung Institute, Imperial College London, United Kingdom;
Imperial College London · GBUniversity of Oxford · GBVanderbilt University · USNational Institute of Environmental Health Sciences · USUniversity of Birmingham · GBUniversity of North Carolina at Chapel Hill · US

Funding

TTP and related proteins in the regulation of gene expressionZIAES090080 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BLACKSHEAR, PERRY J · 2009 to 2025
$52.6M
Novel biochemical and functional targets of PARPR21AI109690 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BOOTHBY, MARK R · 2014 to 2015
$433k
British Heart Foundation FS/11/48/28869British Heart Foundation PG/10/009/28188NIAID NIH HHS R21 AI109690Versus Arthritis 19614
6 · The paper itself

Abstract

Tissue factor (TF) (CD142) is a 47 kDa transmembrane cell surface glycoprotein that triggers the extrinsic coagulation cascade and links thrombosis with inflammation. Although macrophage TF expression is known to be regulated at the RNA level, very little is known about the mechanisms involved. Poly(adenosine 5'-diphosphate [ADP]-ribose)-polymerase (PARP)-14 belongs to a family of intracellular proteins that generate ADP-ribose posttranslational adducts. Functional screening of PARP-14-deficient macrophages mice revealed that PARP-14 deficiency leads to increased TF expression and functional activity in macrophages after challenge with bacterial lipopolysaccharide. This was related to an increase in TF messenger RNA (mRNA) stability. Ribonucleoprotein complex immunoprecipitation and biotinylated RNA pull-down assays demonstrated that PARP-14 forms a complex with the mRNA-destabilizing protein tristetraprolin (TTP) and a conserved adenylate-uridylate-rich element in the TF mRNA 3' untranslated region. TF mRNA regulation by PARP-14 was selective, as tumor necrosis factor (TNF)α mRNA, which is also regulated by TTP, was not altered in PARP-14 deficient macrophages. Consistent with the in vitro data, TF expression and TF activity, but not TNFα expression, were increased in Parp14(-/-) mice in vivo. Our study provides a novel mechanism for the posttranscriptional regulation of TF expression, indicating that this is selectively regulated by PARP-14.

Indexed as

Gene Expression Regulation3' Untranslated RegionsAnimalsLipopolysaccharidesMacrophagesMiceMice, KnockoutPoly(ADP-ribose) PolymerasesRNA StabilityThromboplastinTristetraprolinTumor Necrosis Factor-alpha3' Untranslated RegionsLipopolysaccharidesParp14 protein, mousePoly(ADP-ribose) PolymerasesThromboplastinTristetraprolinTumor Necrosis Factor-alphaZfp36 protein, mouse

Identifiers

PMID25293769
PMCPMC4256914
OpenAlexW2076592490

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.