ArticleiScience2023
SOCS1 regulates a subset of NFκB-target genes through direct chromatin binding and defines macrophage functional phenotypes.
Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 10 citations in OpenAlex.
- AntagomiR-155 hitchhiking on biomimetic yeast microcapsules alleviate atherosclerosis by inhibiting M1-like macrophages.Materials today. Bio · 2026Article
- NF-κB-Dependent Transcriptional Regulation of Piezo1 Mediates Bacterial Clearance on Infected Lung Stiffness.American journal of respiratory cell and molecular biology · 2026Article
- S-nitrosylation of IRF7 induced by NOS1 expression in melanoma suppresses anti-tumor immunity.Cell death & disease · 2026Article
- High-Efficiency Genomic Mapping of Chromatin-Associated Targets with CUT&RUN.Methods in molecular biology (Clifton, N.J.) · 2026Article
- NF-κB-Dependent Transcriptional Regulation of Piezo1 Mediates Bacterial Clearance on Stiffened Lung Matrix.bioRxiv : the preprint server for biology · 2025Article
- Glucocorticoids increase adiposity by stimulating Krüppel-like factor 9 expression in macrophages.Nature communications · 2024Article
- Exploring the role of CITED transcriptional regulators in the control of macrophage polarization.Frontiers in immunology · 2024Review
- Sinensetin Attenuated Macrophagic NLRP3 Inflammasomes FormationACS omega · 2023Article
- Challenges and Future Trends in Atopic Dermatitis.International journal of molecular sciences · 2023Review
- SOCS-JAK-STAT inhibitors and SOCS mimetics as treatment options for autoimmune uveitis, psoriasis, lupus, and autoimmune encephalitis.Frontiers in immunology · 2023Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Suppressor of cytokine signaling-1 (SOCS1) exerts control over inflammation by targeting p65 nuclear factor-κB (NF-κB) for degradation in addition to its canonical role regulating cytokine signaling. We report here that SOCS1 does not operate on all p65 targets equally, instead localizing to a select subset of pro-inflammatory genes. Promoter-specific interactions of SOCS1 and p65 determine the subset of genes activated by NF-κB during systemic inflammation, with profound consequences for cytokine responses, immune cell mobilization, and tissue injury. Nitric oxide synthase-1 (NOS1)-derived nitric oxide (NO) is required and sufficient for the displacement of SOCS1 from chromatin, permitting full inflammatory transcription. Single-cell transcriptomic analysis of NOS1-deficient animals led to detection of a regulatory macrophage subset that exerts potent suppression on inflammatory cytokine responses and tissue remodeling. These results provide the first example of a redox-sensitive, gene-specific mechanism for converting macrophages from regulating inflammation to cells licensed to promote aggressive and potentially injurious inflammation.
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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.