Evidence map›Paper›PMID 40811059›Full record

ArticleCell reports2025

PARP7 inhibition stabilizes STAT1/STAT2 and relieves experimental autoimmune encephalomyelitis in mice.

Jiashu Xu, Tao Yu, Zongwei Yue, Xuan Lu, Yandong Zhang, Lei Wang, Samaneh Shabani Åhrling, Michael R Smith, Yan Chun Li, Jason Matthews and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–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

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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

11 authors.

Jiashu XuDepartment of Chemistry and Chemical Biology, Cornell University, Ithaca, NY 14853, USA; Department of Medicine and Department of Chemistry, The University of Chicago, Chicago, IL 60637, USA.
Tao YuDepartment of Chemistry and Chemical Biology, Cornell University, Ithaca, NY 14853, USA.
Zongwei YueDepartment of Medicine and Department of Chemistry, The University of Chicago, Chicago, IL 60637, USA.
Xuan LuDepartment of Chemistry and Chemical Biology, Cornell University, Ithaca, NY 14853, USA; Department of Medicine and Department of Chemistry, The University of Chicago, Chicago, IL 60637, USA.
Yandong ZhangDepartment of Chemistry and Chemical Biology, Cornell University, Ithaca, NY 14853, USA; Department of Medicine and Department of Chemistry, The University of Chicago, Chicago, IL 60637, USA.
Lei WangDepartment of Medicine, The University of Chicago, Chicago, IL 60637, USA.
Samaneh Shabani ÅhrlingDepartment of Nutrition, Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Sognsvannsveien 9, 0372 Oslo, Norway; Department of Pharmacology and Toxicology, University of Toronto, 1 King's College Circle, Toronto, ON M5S 1A8, Canada.
Michael R SmithDepartment of Chemistry and Chemical Biology, Cornell University, Ithaca, NY 14853, USA.
Yan Chun LiDepartment of Medicine, The University of Chicago, Chicago, IL 60637, USA.
Jason MatthewsDepartment of Nutrition, Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Sognsvannsveien 9, 0372 Oslo, Norway; Department of Pharmacology and Toxicology, University of Toronto, 1 King's College Circle, Toronto, ON M5S 1A8, Canada.
Hening LinDepartment of Chemistry and Chemical Biology, Cornell University, Ithaca, NY 14853, USA; Department of Medicine and Department of Chemistry, The University of Chicago, Chicago, IL 60637, USA; Howard Hughes Medical Institute, Department of Medicine and Department of Chemistry, The University of Chicago, Chicago, IL 60637, USA. Electronic address: linh1@uchicago.edu.

Funding

Design and development of HDAC11-specific chemical inhibitors for disease treatmentsR01AI153110 · NIAID · GEORGE WASHINGTON UNIVERSITY · PI LIN, HENING, MILLER, ROBERT H. · 2021 to 2025
$3.5M
NIAID NIH HHS R01 AI153110
6 · The paper itself

Abstract

The regulation of type I interferon signaling is crucial for precisely tuning the innate immune response to combat pathogen invasions, fight cancer, and prevent autoimmune diseases. PARP7, a mono-ADP-ribosyltransferase also called TiPARP (tetrachlorodibenzo-p-dioxin [TCDD]-inducible PARP), is reported to inhibit the production of type I interferons. Here, we find that PARP7 suppresses type I interferon signaling instead of interferon production. PARP7 ADP-ribosylates and promotes the ubiquitination of signal transducer and activator of transcription 1 (STAT1) and STAT2, which recruits p62 to promote the degradation of STAT1 and STAT2 through autophagy. By reducing STAT1 and STAT2 levels, PARP7 decreases type I interferon signaling. We further show that the inhibition of PARP7 promotes type I interferon signaling and relieves experimental autoimmune encephalomyelitis (EAE) symptoms in mice. Our findings revealed a molecular mechanism via which PARP7 suppresses type I interferon signaling, offering insights into the immune-modulatory function of PARP7 and suggesting PARP7 inhibition as a potential treatment strategy for multiple sclerosis.

Indexed as

ADP Ribose TransferasesEncephalomyelitis, Autoimmune, ExperimentalPoly(ADP-ribose) PolymerasesSTAT1 Transcription FactorSTAT2 Transcription FactorAnimalsFemaleHumansInterferon Type IMiceMice, Inbred C57BLProtein StabilitySignal TransductionUbiquitinationADP Ribose TransferasesInterferon Type IPoly(ADP-ribose) PolymerasesStat1 protein, mouseSTAT1 Transcription FactorStat2 protein, mouseSTAT2 Transcription FactorADP-ribosylationautophagyCP: Molecular biologyCP: NeuroscienceEAEmultiple sclerosisPARP7STAT1STAT2TiPARPtype I interferon signalingubiquitination

Identifiers

PMID40811059
PMCPMC12509220

What OpenQuestion 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 OpenQuestion graph.