ReviewGrowth factors (Chur, Switzerland)2012
The biology and mechanism of action of suppressor of cytokine signaling 3.
Review in Growth factors (Chur, Switzerland), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.
- The Role of DNA Methylation and Histone Modification in Periodontal Disease: A Systematic Review.International journal of molecular sciences · 2020Pooled it
- TGF-β-induced epigenetic deregulation of SOCS3 facilitates STAT3 signaling to promote fibrosis.The Journal of clinical investigation · 2020Trial
- Review
- Genome-wide CRISPR screen identifies a cytokine-enhancer circuit driving HIF-2α activation in renal cancer.The Journal of clinical investigation · 2026Article
- Receptor engineering constitutes feedback control and robustness of IL-23R signaling and highlights importance of intracellular cytokine receptor signaling motifs.Cell communication and signaling : CCS · 2026Article
- Breast Cancer Bone Metastasis: Novel Prognostic Biomarkers Identified.Phenomics (Cham, Switzerland) · 2025Article
- Hypoferremic Response to Chronic Inflammation Is Controlled via the Hemojuvelin/Hepcidin/Ferroportin Axis and Does Not Involve Hepcidin-Independent Regulation of Fpn mRNA.American journal of hematology · 2025Article
- Cullin-5 controls the number of megakaryocyte-committed stem cells to prevent thrombocytosis in mice.Blood · 2025Article
- FGFR antagonists restore defective mandibular bone repair in a mouse model of osteochondrodysplasia.Bone research · 2025Article
- Exploring Epigenetic Mechanisms in Aggressive Periodontitis; Unraveling the Molecular Dynamics of Disease Progression: A Narrative Review.Iranian journal of medical sciences · 2024Review
- E3 ligase SOCS3 regulates NOD2 expression by ubiquitin proteasome system in lung cancer progression.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Suppressor of Cytokine Signaling-3 Gene Polymorphisms and the Risk of Hepatocellular Carcinoma in Chronic Hepatitis C Patients in Egypt.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- Myeloid FTH1 Deficiency Protects Mice From Colitis and Colitis-associated Colorectal Cancer via Reducing DMT1-Imported Iron and STAT3 Activation.Inflammatory bowel diseases · 2023Article
- SOCS3 Silencing Promotes Activation of Vocal Fold Fibroblasts via JAK2/STAT3 Signaling Pathway.Inflammation · 2023Article
- Oncogenic role of microRNA-19b-3p-mediated SOCS3 in glioma through activation of JAK-STAT pathway.Metabolic brain disease · 2023Article
- Suppressor of cytokine signaling 3-derived peptide as a therapeutic for inflammatory and oxidative stress-induced damage to the retina.Molecular vision · 2023Article
- Oral Cancer Cells Release Vesicles that Cause Pain.Advanced biology · 2022Article
- A Genome-Wide CRISPR Screen Identifies Factors Regulating Pluripotency Exit in Mouse Embryonic Stem Cells.Cells · 2022Article
- A review of granulocyte colony-stimulating factor receptor signaling and regulation with implications for cancer.Frontiers in oncology · 2022Review
- "Big Data" Approaches for Prevention of the Metabolic Syndrome.Frontiers in genetics · 2022Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Suppressors of cytokine signaling 3 (SOCS3) has been shown to be an important and non-redundant feedback inhibitor of several cytokines including leukemia inhibitory factor, IL-6, IL-11, Ciliary neurotrophic factor (CNTF), leptin, and granulocyte colony-stimulating factor (G-CSF). Loss of SOCS3 in vivo has profound effects on placental development, inflammation, fat-induced weight gain, and insulin sensitivity. SOCS3 expression is induced by Janus kinase (JAK)/signal transducers and activators of transcription (STAT) signaling and it then binds to specific cytokine receptors (including gp130, G-CSF, and leptin receptors). SOCS3 then inhibits JAK/STAT signaling in two distinct ways. First, SOCS3 is able to directly inhibit the catalytic activity of JAK1, JAK2, or TYK2 while remaining bound to the cytokine receptor. Second, SOCS3 recruits elongins B/C and Cullin5 to generate an E3 ligase that ubiquitinates both JAK and cytokine receptor targeting them for proteasomal degradation. Detailed in vivo studies have revealed that SOCS3 action not only limits the duration of cytokine signaling to prevent overactivity but it is also important in maintaining the specificity of cytokine signaling.
Indexed as
Identifiers
What OpenQuestion holds
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.