ArticleThe EMBO journal1999
Mutational analyses of the SOCS proteins suggest a dual domain requirement but distinct mechanisms for inhibition of LIF and IL-6 signal transduction.
Article in The EMBO journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.
What it found
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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.
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.
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Who cites it
118 citing papers in PubMed, 421 citations in OpenAlex.
- SOCS1 Inhibits IL-6-Induced CD155 Overexpression in Lung Adenocarcinoma.International journal of molecular sciences · 2024Article
- Diverse signaling mechanisms and heterogeneity of astrocyte reactivity in Alzheimer's disease.Journal of neurochemistry · 2024Review
- Unravelling the druggability and immunological roles of the SOCS-family proteins.Frontiers in immunology · 2024Review
- SOCS1 and SOCS3 as key checkpoint molecules in the immune responses associated to skin inflammation and malignant transformation.Frontiers in immunology · 2024Review
- SOCS1 is a critical checkpoint in immune homeostasis, inflammation and tumor immunity.Frontiers in immunology · 2024Review
- Role of SOCS and VHL Proteins in Neuronal Differentiation and Development.International journal of molecular sciences · 2023Review
- The Role of the JAK/STAT Signaling Pathway in the Pathogenesis of Alzheimer's Disease: New Potential Treatment Target.International journal of molecular sciences · 2023Review
- Leukemia Inhibitory Factor: An Important Cytokine in Pathologies and Cancer.Biomolecules · 2022Review
- Microtubule-dependent mechanism of anti-inflammatory effect of SOCS1 in endothelial dysfunction and lung injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Proteomimetics of Natural Regulators of JAK-STAT Pathway: Novel Therapeutic Perspectives.Frontiers in molecular biosciences · 2021Review
- MicroRNA-653-5p Promotes Gastric Cancer Proliferation and Metastasis by Targeting the SOCS6-STAT3 Pathway.Frontiers in molecular biosciences · 2021Article
- Article
- Severe type I interferonopathy and unrestrained interferon signaling due to a homozygous germline mutation inScience immunology · 2019Article
- SOCS1 and its Potential Clinical Role in Tumor.Pathology oncology research : POR · 2019Review
- Review
- Interaction of suppressor of cytokine signalling 3 with cavin-1 links SOCS3 function and cavin-1 stability.Nature communications · 2018Article
- The role of JAK-STAT signaling pathway and its regulators in the fate of T helper cells.Cell communication and signaling : CCS · 2017Review
- SOCS Proteins as Regulators of Inflammatory Responses Induced by Bacterial Infections: A Review.Frontiers in microbiology · 2017Review
- Article
- Transcellular delivery of vesicular SOCS proteins from macrophages to epithelial cells blunts inflammatory signaling.The Journal of experimental medicine · 2015Article
58 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
10 authors at 1 institution in 1 country.
Funding
Abstract
SOCS-1 (suppressor of cytokine signaling-1) is a representative of a family of negative regulators of cytokine signaling (SOCS-1 to SOCS-7 and CIS) characterized by a highly conserved C-terminal SOCS box preceded by an SH2 domain. This study comprehensively examined the ability of several SOCS family members to negatively regulate the gp130 signaling pathway. SOCS-1 and SOCS-3 inhibited both interleukin-6 (IL-6)- and leukemia inhibitory factor (LIF)-induced macrophage differentiation of murine monocytic leukemic M1 cells and LIF induction of a Stat3-responsive reporter construct in 293T fibroblasts. Deletion of amino acids 51-78 in the N-terminal region of SOCS-1 prevented inhibition of LIF signaling. The SOCS-1 and SOCS-3 N-terminal regions were functionally interchangeable, but this did not extend to other SOCS family members. Mutation of SH2 domains abrogated the ability of both SOCS-1 and SOCS-3 to inhibit LIF signal transduction. Unlike SOCS-1, SOCS-3 was unable to inhibit JAK kinase activity in vitro, suggesting that SOCS-1 and SOCS-3 act on the JAK-STAT pathway in different ways. Thus, although inhibition of signaling by SOCS-1 and SOCS-3 requires both the SH2 and N-terminal domains, their mechanisms of action appear to be biochemically different.
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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.