ArticleFrontiers in immunology2018
STAT3 Cooperates With Phospholipid Scramblase 2 to Suppress Type I Interferon Response.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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.
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Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
- The function and mechanism of protein acylation in the regulation of viral infection.Virulence · 2025Review
- Protein lipidation in the tumor microenvironment: enzymology, signaling pathways, and therapeutics.Molecular cancer · 2025Review
- zDHHC-Mediated S-Palmitoylation in Skin Health and Its Targeting as a Treatment Perspective.International journal of molecular sciences · 2025Review
- STAT3 Increases CVB3 Replication and Acute Pancreatitis and Myocarditis Pathology via Impeding Nuclear Translocation of STAT1 and Interferon-Stimulated Gene Expression.International journal of molecular sciences · 2024Article
- Inhibition of insulin-like growth factors increases production of CXCL9/10 by macrophages and fibroblasts and facilitates CD8Frontiers in immunology · 2024Article
- Capsaicin functions as a selective degrader of STAT3 to enhance host resistance to viral infection.Acta pharmacologica Sinica · 2023Article
- Interferon Signaling in the Endometrium and in Endometriosis.Biomolecules · 2022Review
- IFN-β1b induces OAS3 to inhibit EV71 via IFN-β1b/JAK/STAT1 pathway.Virologica Sinica · 2022Article
- Circulating microRNA sequencing revealed miRNome patterns in hematology and oncology patients aiding the prognosis of invasive aspergillosis.Scientific reports · 2022Article
- FTO Suppresses STAT3 Activation and Modulates Proinflammatory Interferon-Stimulated Gene Expression.Journal of molecular biology · 2022Article
- Phospholipid Scramblases: Role in Cancer Progression and Anticancer Therapeutics.Frontiers in genetics · 2022Review
- Targeting macrophage priming by polyphyllin VII triggers anti-tumor immunity via STING-governed cytotoxic T-cell infiltration in lung cancer.Scientific reports · 2020Article
- The Dynamic Interface of Viruses with STATs.Journal of virology · 2020Review
- Targeting STAT3 in Cancer Immunotherapy.Molecular cancer · 2020Review
- Genetic Analyses of Contributions of Viral Interleukin-6 Interactions and Signaling to Human Herpesvirus 8 Productive Replication.Journal of virology · 2020Article
- Lyssavirus P-protein selectively targets STAT3-STAT1 heterodimers to modulate cytokine signalling.PLoS pathogens · 2020Article
- Type I interferon limits mast cell-mediated anaphylaxis by controlling secretory granule homeostasis.PLoS biology · 2019Article
- STAT3 Regulates the Type I IFN-Mediated Antiviral Response by Interfering with the Nuclear Entry of STAT1.International journal of molecular sciences · 2019Article
- Modulation of Mast Cell Reactivity by Lipids: The Neglected Side of Allergic Diseases.Frontiers in immunology · 2019Review
- Fine-Tuning of Type I Interferon Response by STAT3.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type I interferon (IFN-I) is a pluripotent cytokine that modulates innate and adaptive immunity. We have previously shown that STAT3 suppresses IFN-I response in a manner dependent on its N-terminal domain (NTD), but independent of its DNA-binding and transactivation ability. Using the yeast two-hybrid system, we have identified phospholipid scramblase 2 (PLSCR2) as a STAT3 NTD-binding partner and a suppressor of IFN-I response. Overexpression of PLSCR2 attenuates ISRE-driven reporter activity, which is further aggravated by co-expression of STAT3. Moreover, PLSCR2 deficiency enhances IFN-I-induced gene expression and antiviral activity without affecting the activation or nuclear translocation of STAT1 and STAT2 or the assembly of ISGF3 complex. Instead, PLSCR2 impedes promoter occupancy by ISGF3, an effect further intensified by the presence of STAT3. Moreover, palmitoylation of PLSCR2 is required for its binding to STAT3 and for this suppressive activity. In addition to STAT3, PLSCR2 also interacts with STAT2, which facilitates the suppressive effect on ISGF3-mediated transcriptional activity. Together, these results define the role of a novel STAT3-PLSCR2 axis in fine-tuning IFN-I response.
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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.