In one paragraphArticle in Viruses, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
16 authors.
Abbey N WarrenCenter for Virus-Host-Innate-Immunity, RBHS Institute for Infectious and Inflammatory Diseases, and Department of Medicine, New Jersey Medical School, Rutgers University, Newark, NJ 07103, USA.ORCID 0000-0002-5838-0208 Maria Gonzalez-OrozcoDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Ivan KuzminDepartment of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Sreeja ParameswaranCenter for Autoimmune Genomics and Etiology, Division of Allergy and Immunology, Cincinnati Children's Hospital, Cincinnati, OH 45229, USA.ORCID 0009-0002-3631-3669 Ruben Soto AcostaDepartment of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Birte KalveramDepartment of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Sarah van TolDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Adam HageDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.ORCID 0000-0001-7668-892X Padmanava BeheraCenter for Virus-Host-Innate-Immunity, RBHS Institute for Infectious and Inflammatory Diseases, and Department of Medicine, New Jersey Medical School, Rutgers University, Newark, NJ 07103, USA.
Yoatzin Peñaflor-TellezCenter for Virus-Host-Innate-Immunity, RBHS Institute for Infectious and Inflammatory Diseases, and Department of Medicine, New Jersey Medical School, Rutgers University, Newark, NJ 07103, USA.ORCID 0009-0006-9494-3748 Maria I GiraldoDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
William RussellDepartment of Biochemistry and Molecular Biology, The University of Texas Medical Branch at Galveston, Galveston, TX 77555, USA.ORCID 0000-0003-1931-4555 Matthew T WeirauchCenter for Autoimmune Genomics and Etiology, Division of Allergy and Immunology, Cincinnati Children's Hospital, Cincinnati, OH 45229, USA.ORCID 0000-0001-7977-9122 Alexander FreibergDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.ORCID 0000-0001-8413-8960 Alexander BukreyevDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Ricardo RajsbaumCenter for Virus-Host-Innate-Immunity, RBHS Institute for Infectious and Inflammatory Diseases, and Department of Medicine, New Jersey Medical School, Rutgers University, Newark, NJ 07103, USA.ORCID 0000-0002-5058-5444 Funding
Research Project 3: Role of Posttranslational Protein Modifications in the Pathogenesis of Ebola Virus DiseaseP01AI150585 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI BUKREYEV, ALEXANDER · 2021 to 2025
$11.3MRegulation of Ebola virus replication by the host ubiquitin systemR01AI134907 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI GIRALDO, MARIA ISABEL · 2018 to 2022
$3.1MNational Institute of Allergy and Infectious Diseases P01AI150585National Institute of Allergy and Infectious Diseases R01AI134907NIAID NIH HHS P01 AI150585NIAID NIH HHS R01 AI134907
6 · The paper itselfAbstract
Ebola virus disease (EVD) is characterized by immune dysregulation and damaging hyperinflammation. We aimed to characterize the signaling pathways and regulatory mechanisms dysregulated during EVD. To avoid hyperinflammation, innate immune signaling is regulated by post-translational modifications (PTMs), including protein phosphorylation. Here, we show that the protein tyrosine phosphatase nonreceptor type 13 (PTPN13) negatively regulates Interferon (IFN)-β while also positively regulating the neutrophil chemoattractant CXCL1. Using vectors encoding IRF3 with mutations on phosphorylation sites, we identified Y292 on IRF3 as a PTPN13 target of dephosphorylation. Knockout of PTPN13 increased IRF3 phosphorylation and expression of IFNβ and IFN-stimulated genes (ISGs) following poly(I:C) stimulation. Intriguingly, depletion of PTPN13 during Ebola virus (EBOV) infection resulted in decreased IFNβ and ISG induction at later time points post-infection, which correlated with increased viral titers. We identified PTPN13-mediated dephosphorylation of the viral protein VP35 as one potential mechanism inhibiting virus replication. Additionally, the induction of inflammatory chemokines, including CXCL1, decreased in PTPN13 knockout cells late during EBOV infection. These effects could be explained by increased phosphorylation of the regulatory p85 subunit of PI3K. Dephosphorylation of p85 promotes its degradation, subsequently enhancing PI3K kinase activity and downstream signaling via AKT. Together, our study suggests that PTPN13 is involved in immune regulation and efficient antiviral responses by dephosphorylation of IRF3, EBOV-VP35 and PI3K-p85.
Indexed as
EbolavirusHemorrhagic Fever, EbolaInterferon Regulatory Factor-3Phosphatidylinositol 3-KinasesAnimalsChemokine CXCL1HumansImmunity, InnateInterferon-betaPhosphorylationProtein Processing, Post-TranslationalSignal TransductionVirus ReplicationChemokine CXCL1Interferon-betaInterferon Regulatory Factor-3IRF3 protein, humanPhosphatidylinositol 3-KinasesEbola virus (EBOV)innate immune responsephosphorylationPI(3)K pathwayprotein tyrosine phosphatasetype-I interferons (IFN-I)
Identifiers
PMID42515581
PMCPMC13431591
What OpenQuestion holds
Textmetadata
LicenceCC BY
Read underepoch 390