ArticleNature communications2014
PARP13 regulates cellular mRNA post-transcriptionally and functions as a pro-apoptotic factor by destabilizing TRAILR4 transcript.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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.
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.
Who cites it
75 citing papers in PubMed, 5 citations in OpenAlex.
- ZAP targets aberrant mRNA transcripts encoding proteins with defective signal peptides for degradation.The EMBO journal · 2026Article
- Roles of ADP-Ribosyltransferases in Cancer.Oncology research · 2026Review
- PARPs and PARP inhibitors: molecular mechanisms and clinical applications.Molecular biomedicine · 2025Review
- Targeting MARylation and DePARylation in Cancer Therapy: New Promising Therapeutic Opportunities.Cancers · 2025Review
- Non canonical BRCA1 promotes cell survival via modulating PARP13-mediated SEC61G mRNA decay.Oncogenesis · 2025Article
- Review
- HIV-2 evades restriction by ZAP through adaptations in the U3 LTR region despite increased CpG levels.Nucleic acids research · 2025Article
- PARP9-PARP13-PARP14 axis tunes colorectal cancer response to radiotherapy.Journal of experimental & clinical cancer research : CR · 2025Article
- Modulation of host gene expression by the zinc finger antiviral protein.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Regulation of stress granule maturation and dynamics by poly(ADP-ribose) interaction with PARP13.Nature communications · 2025Article
- Endogenous ZAP is associated with altered Zika virus infection phenotype.Virology journal · 2024Article
- Foot-and-mouth disease virus (FMDV) negatively regulates ZFP36 protein expression to alleviate its antiviral activity.Journal of virology · 2024Article
- PARP enzymes and mono-ADP-ribosylation: advancing the connection from interferon-signalling to cancer biology.Expert reviews in molecular medicine · 2024Review
- Positive selection analyses identify a single WWE domain residue that shapes ZAP into a more potent restriction factor against alphaviruses.PLoS pathogens · 2024Article
- Mono-ADP-ribosylation, a MARylationmultifaced modification of protein, DNA and RNA: characterizations, functions and mechanisms.Cell death discovery · 2024Review
- Article
- Versatility of the Zinc-Finger Antiviral Protein (ZAP) As a Modulator of Viral Infections.International journal of biological sciences · 2024Review
- Endogenous ZAP affects Zika virus RNA interactome.RNA biology · 2024Article
- Immunofluorescence-Verified Sphingolipid Signatures Indicate Improved Prognosis in Liver Cancer Patients.Journal of Cancer · 2024Article
- Antiviral Activity of Zinc Finger Antiviral Protein (ZAP) in Different Virus Families.Pathogens (Basel, Switzerland) · 2023Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Poly(ADP-ribose) polymerase-13 (PARP13/ZAP/ZC3HAV1) is an antiviral factor, active against specific RNA viruses such as murine leukaemia virus, Sindbis virus and human immunodeficiency virus. During infection, PARP13 binds viral RNA via its four CCCH-type zinc-finger domains and targets it for degradation by recruiting cellular messenger RNA (mRNA) decay factors such as the exosome complex and XRN1. Here we show that PARP13 binds to and regulates cellular mRNAs in the absence of viral infection. Knockdown of PARP13 results in the misregulation of hundreds of transcripts. Among the most upregulated transcripts is TRAILR4 that encodes a decoy receptor for TRAIL-a pro-apoptotic cytokine that is a promising target for the therapeutic inhibition of cancers. PARP13 destabilizes TRAILR4 mRNA post-transcriptionally in an exosome-dependent manner by binding to a region in its 3' untranslated region. As a consequence, PARP13 represses TRAILR4 expression and increases cell sensitivity to TRAIL-mediated apoptosis, acting as a key regulator of the cellular response to TRAIL.
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Identifiers
What OpenQuestion holds
Registered trials
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.