ArticleNature communications2016
PARP9 and PARP14 cross-regulate macrophage activation via STAT1 ADP-ribosylation.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05215808 (A First-in-Human, Randomized, Placebo-Controlled, Phase 1 Single and Multiple Ascending Dose Study to Assess the Safety and Pharmacokinetics of RBN-3143 in Healthy Subjects and as Open-Label in Patients With Atopic Dermatitis Subjects), which is not on this map. Cited by 192 papers, 1 of them a synthesis that pooled it.
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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.
A First-in-Human, Randomized, Placebo-Controlled, Phase 1 Single and Multiple Ascending Dose Study to Assess the Safety and Pharmacokinetics of RBN-3143 in Healthy Subjects and as Open-Label in Patients With Atopic Dermatitis Subjects
Who cites it
192 citing papers in PubMed, 1 synthesis or guideline pooled it, 302 citations in OpenAlex.
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- First-in-Human Phase 1 Study to Evaluate the Clinical Pharmacology Properties of RBN-3143, a Novel Inhibitor of Mono-Adenosine Diphosphate Ribosyltransferase-PARP14.Clinical pharmacology in drug development · 2025Trial
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- Nuclear RSK1 mediates interferon-γ-induced proinflammatory activation in human primary macrophages and humanized mice.Science advances · 2026Article
- Structure, function, regulation, evolution, and therapeutic implications of PARP14.Genes & development · 2026Review
- Decoding ulcerative colitis pathogenesis through transcriptomics: from dysregulated gene networks to targeted intervention strategies.Journal of translational autoimmunity · 2026Article
- Platelets as immune sensors: monitoring immune dynamics and diagnosing disease states across multiple disorders.EBioMedicine · 2026Article
- Epigenomic subtypes of late-onset Alzheimer's disease reveal distinct microglial signatures.Acta neuropathologica · 2026Article
- Exacerbated salmonellosis in poly(ADP-ribose) polymerase 14-deficient mice.Microbiology spectrum · 2026Article
- HeptaTB Dx: a diagnostic model leveraging cuproptosis-ferroptosis crosstalk for distinguishing latent from active tuberculosis.Microbiology spectrum · 2026Article
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- Altered nicotinamide adenine dinucleotide metabolism drives cartilage degeneration and osteoarthritis.Clinical and translational medicine · 2025Article
- ADP-Ribosylation in Experimental Atherosclerosis: A Potential Link Between Dyslipidemia and Inflammation in Cardiovascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Tipping the PARylation scale: Dysregulation of PAR signaling in Huntington and neurodegenerative diseases.Journal of Huntington's disease · 2025Review
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- Identification of key genes as diagnostic biomarkers for IBD using bioinformatics and machine learning.Journal of translational medicine · 2025Article
- Systematic Identification of Mitochondrial Signatures in Alzheimer's Disease and Inflammatory Bowel Disease.Molecular neurobiology · 2025Article
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- Vertical transmission of Leishmania donovani with placental degeneration in the pregnant mouse model of visceral leishmaniasis.PLoS neglected tropical diseases · 2025Article
132 more citing papers are in PubMed but not listed here.
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Authors and funding
19 authors at 2 institutions in 1 country.
Funding
Abstract
Despite the global impact of macrophage activation in vascular disease, the underlying mechanisms remain obscure. Here we show, with global proteomic analysis of macrophage cell lines treated with either IFNγ or IL-4, that PARP9 and PARP14 regulate macrophage activation. In primary macrophages, PARP9 and PARP14 have opposing roles in macrophage activation. PARP14 silencing induces pro-inflammatory genes and STAT1 phosphorylation in M(IFNγ) cells, whereas it suppresses anti-inflammatory gene expression and STAT6 phosphorylation in M(IL-4) cells. PARP9 silencing suppresses pro-inflammatory genes and STAT1 phosphorylation in M(IFNγ) cells. PARP14 induces ADP-ribosylation of STAT1, which is suppressed by PARP9. Mutations at these ADP-ribosylation sites lead to increased phosphorylation. Network analysis links PARP9-PARP14 with human coronary artery disease. PARP14 deficiency in haematopoietic cells accelerates the development and inflammatory burden of acute and chronic arterial lesions in mice. These findings suggest that PARP9 and PARP14 cross-regulate macrophage activation.
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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.