ArticleMolecular and cellular biology1999
SOCS-3 is tyrosine phosphorylated in response to interleukin-2 and suppresses STAT5 phosphorylation and lymphocyte proliferation.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 264 citations in OpenAlex.
- Conditioned medium from cultured cementoblasts upregulates amelotin gene expression via the SOCS3 signaling pathway.Journal of periodontal & implant science · 2025Article
- Cytokines in Focus: IL-2 and IL-15 in NK Adoptive Cell Cancer Immunotherapy.Immune network · 2025Review
- Comprehensive snapshots of natural killer cells functions, signaling, molecular mechanisms and clinical utilization.Signal transduction and targeted therapy · 2024Review
- Zfp36l1 establishes the high-affinity CD8 T-cell response by directly linking TCR affinity to cytokine sensing.European journal of immunology · 2024Article
- Early transcriptomic changes at the skin interface during Powassan virus transmission byFrontiers in immunology · 2024Article
- IL-6 prevents Th2 cell polarization by promoting SOCS3-dependent suppression of IL-2 signaling.Cellular & molecular immunology · 2023Article
- Role of SOCS and VHL Proteins in Neuronal Differentiation and Development.International journal of molecular sciences · 2023Review
- Potential Natural Biomolecules Targeting JAK/STAT/SOCS Signaling in the Management of Atopic Dermatitis.Molecules (Basel, Switzerland) · 2022Review
- Organophosphorus Pesticides as Modulating Substances of Inflammation through the Cholinergic Pathway.International journal of molecular sciences · 2022Review
- How GRAIL controls Treg function to maintain self-tolerance.Frontiers in immunology · 2022Article
- SOCS proteins and their roles in the development of glioblastoma.Oncology letters · 2022Review
- Extracellular Vesicles: Potential Mediators of Psychosocial Stress Contribution to Osteoporosis?International journal of molecular sciences · 2021Review
- Long noncoding RNA UCA1 regulates HCV replication and antiviral response via miR-145-5p/SOCS7/IFN pathway.International journal of biological sciences · 2021Article
- SOCS3 is a suppressor of γc cytokine signaling and constrains generation of murine Foxp3European journal of immunology · 2020Article
- Dissociating STAT4 and STAT5 Signaling Inhibitory Functions of SOCS3: Effects on CD8 T Cell Responses.ImmunoHorizons · 2019Article
- Potential of C1QTNF1-AS1 regulation in human hepatocellular carcinoma.Molecular and cellular biochemistry · 2019Article
- Nanoparticles Targeting STATs in Cancer Therapy.Cells · 2019Review
- C1QTNF1-AS1 regulates the occurrence and development of hepatocellular carcinoma by regulating miR-221-3p/SOCS3.Hepatology international · 2019Article
- Constitutive STAT3 phosphorylation and IL-6/IL-10 co-expression are associated with impaired T-cell function in tuberculosis patients.Cellular & molecular immunology · 2019Article
- T Regulatory Cells From Non-obese Diabetic Mice Show Low Responsiveness to IL-2 Stimulation and Exhibit Differential Expression of Anergy-Related and Ubiquitination Factors.Frontiers in immunology · 2019Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Members of the recently discovered SOCS/CIS/SSI family have been proposed as regulators of cytokine signaling, and while targets and mechanisms have been suggested for some family members, the precise role of these proteins remains to be defined. To date no SOCS proteins have been specifically implicated in interleukin-2 (IL-2) signaling in T cells. Here we report SOCS-3 expression in response to IL-2 in both T-cell lines and human peripheral blood lymphocytes. SOCS-3 protein was detectable as early as 30 min following IL-2 stimulation, while CIS was seen only at low levels after 2 h. Unlike CIS, SOCS-3 was rapidly tyrosine phosphorylated in response to IL-2. Tyrosine phosphorylation of SOCS-3 was observed upon coexpression with Jak1 and Jak2 but only weakly with Jak3. In these experiments, SOCS-3 associated with Jak1 and inhibited Jak1 phosphorylation, and this inhibition was markedly enhanced by the presence of IL-2 receptor beta chain (IL-2Rbeta). Moreover, following IL-2 stimulation of T cells, SOCS-3 was able to interact with the IL-2 receptor complex, and in particular tyrosine phosphorylated Jak1 and IL-2Rbeta. Additionally, in lymphocytes expressing SOCS-3 but not CIS, IL-2-induced tyrosine phosphorylation of STAT5b was markedly reduced, while there was only a weak effect on IL-3-mediated STAT5b tyrosine phosphorylation. Finally, proliferation induced by both IL-2- and IL-3 was significantly inhibited in the presence of SOCS-3. The findings suggest that when SOCS-3 is rapidly induced by IL-2 in T cells, it acts to inhibit IL-2 responses in a classical negative feedback loop.
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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.