Evidence map›Paper›PMID 38834853›Full record

ArticleThe EMBO journal2024

PARP14 and PARP9/DTX3L regulate interferon-induced ADP-ribosylation.

Pulak Kar, Chatrin Chatrin, Nina Đukić, Osamu Suyari, Marion Schuller, Kang Zhu, Evgeniia Prokhorova, Nicolas Bigot, Domagoj Baretić, Juraj Ahel and 9 more

Erratum issuedAbstract read
In one paragraph

Article in The EMBO journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
–field-weighted citation impact
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

38 citing papers in PubMed.

  1. Article
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  11. Oncology research · 2026
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  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. The Mac1 ADP-ribosylhydrolase is a Therapeutic Target for SARS-CoV-2.bioRxiv : the preprint server for biology · 2025
    Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors.

Pulak Kar *Sir William Dunn School of Pathology, University of Oxford, Oxford, OX1 3RE, UK.
Chatrin Chatrin *Sir William Dunn School of Pathology, University of Oxford, Oxford, OX1 3RE, UK.
Nina Đukić *Sir William Dunn School of Pathology, University of Oxford, Oxford, OX1 3RE, UK.ORCID http://orcid.org/0009-0004-6120-6421
Osamu SuyariSir William Dunn School of Pathology, University of Oxford, Oxford, OX1 3RE, UK.ORCID http://orcid.org/0009-0008-3258-8722
Marion SchullerSir William Dunn School of Pathology, University of Oxford, Oxford, OX1 3RE, UK.
Kang ZhuSir William Dunn School of Pathology, University of Oxford, Oxford, OX1 3RE, UK.ORCID http://orcid.org/0000-0003-2623-3331
Evgeniia ProkhorovaSir William Dunn School of Pathology, University of Oxford, Oxford, OX1 3RE, UK.
Nicolas BigotUniv Rennes, CNRS, IGDR (Institut de génétique et développement de Rennes) - UMR 6290, BIOSIT - UMS3480, F-35000, Rennes, France.ORCID http://orcid.org/0000-0002-4247-0217
Domagoj BaretićSir William Dunn School of Pathology, University of Oxford, Oxford, OX1 3RE, UK.
Juraj AhelResearch Institute of Molecular Pathology (IMP), Vienna BioCenter, Vienna, Austria.ORCID http://orcid.org/0000-0003-0293-1063
Jonas Damgaard ElsborgProteomics Program, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, 2200, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-1506-4280
Michael L NielsenProteomics Program, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, 2200, Copenhagen, Denmark.
Tim ClausenResearch Institute of Molecular Pathology (IMP), Vienna BioCenter, Vienna, Austria.
Sébastien HuetUniv Rennes, CNRS, IGDR (Institut de génétique et développement de Rennes) - UMR 6290, BIOSIT - UMS3480, F-35000, Rennes, France.
Mario NiepelRibon Therapeutics, Cambridge, MA, 02140, USA.ORCID http://orcid.org/0000-0003-1415-6295
Sumana SanyalSir William Dunn School of Pathology, University of Oxford, Oxford, OX1 3RE, UK.ORCID http://orcid.org/0000-0002-6230-5366
Dragana AhelSir William Dunn School of Pathology, University of Oxford, Oxford, OX1 3RE, UK.
Rebecca SmithSir William Dunn School of Pathology, University of Oxford, Oxford, OX1 3RE, UK. rebecca.smith@path.ox.ac.uk.ORCID http://orcid.org/0000-0002-1658-5635
Ivan AhelSir William Dunn School of Pathology, University of Oxford, Oxford, OX1 3RE, UK. ivan.ahel@path.ox.ac.uk.ORCID http://orcid.org/0000-0002-9446-3756

Funding

Agence Nationale de la Recherche (ANR) ANR-22-CE12-0039Fondation ARC pour la Recherche sur le Cancer (ARC) ARCPJA2022060005190Ligue Contre le Cancer (French League Against Cancer) CD53Ovarian Cancer Research Alliance (OCRA) 813369Oxford University Challenge Seed Fund USCF 456UKRI | Biotechnology and Biological Sciences Research Council (BBSRC) BB/R007195/1UKRI | Biotechnology and Biological Sciences Research Council (BBSRC) BB/W016613/1Wellcome TrustWellcome Trust 210634Wellcome Trust 223107
6 · The paper itself

Abstract

PARP-catalysed ADP-ribosylation (ADPr) is important in regulating various cellular pathways. Until recently, PARP-dependent mono-ADP-ribosylation has been poorly understood due to the lack of sensitive detection methods. Here, we utilised an improved antibody to detect mono-ADP-ribosylation. We visualised endogenous interferon (IFN)-induced ADP-ribosylation and show that PARP14 is a major enzyme responsible for this modification. Fittingly, this signalling is reversed by the macrodomain from SARS-CoV-2 (Mac1), providing a possible mechanism by which Mac1 counteracts the activity of antiviral PARPs. Our data also elucidate a major role of PARP9 and its binding partner, the E3 ubiquitin ligase DTX3L, in regulating PARP14 activity through protein-protein interactions and by the hydrolytic activity of PARP9 macrodomain 1. Finally, we also present the first visualisation of ADPr-dependent ubiquitylation in the IFN response. These approaches should further advance our understanding of IFN-induced ADPr and ubiquitin signalling processes and could shed light on how different pathogens avoid such defence pathways.

Indexed as

ADP-RibosylationInterferonsPoly(ADP-ribose) PolymerasesUbiquitin-Protein LigasesCOVID-19HEK293 CellsHumansNeoplasm ProteinsSARS-CoV-2Signal TransductionUbiquitinationDTX3L protein, humanInterferonsNeoplasm ProteinsPARP14 protein, humanPARP9 protein, humanPoly(ADP-ribose) PolymerasesUbiquitin-Protein LigasesADP-ribosylationImmune ResponseInterferon ResponseSARS-CoV2Ubiquitin

Identifiers

PMID38834853
PMCPMC11251020

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.