The DOI matches its Crossref record; 178 of the 179 references it cites were found in a registry or an index.
SOCS3, a Major Regulator of Infection and Inflammation
Open accessAbstract
In this review, we describe the role of suppressor of cytokine signaling-3 (SOCS3) in modulating the outcome of infections and autoimmune diseases as well as the underlying mechanisms. SOCS3 regulates cytokine or hormone signaling usually preventing, but in some cases aggravating, a variety of diseases. A main role of SOCS3 results from its binding to both the JAK kinase and the cytokine receptor, which results in the inhibition of STAT3 activation. Available data also indicate that SOCS3 can regulate signaling via other STATs than STAT3 and also controls cellular pathways unrelated to STAT activation. SOCS3 might either act directly by hampering JAK activation or by mediating the ubiquitination and subsequent proteasome degradation of the cytokine/growth factor/hormone receptor. Inflammation and infection stimulate SOCS3 expression in different myeloid and lymphoid cell populations as well as in diverse non-hematopoietic cells. The accumulated data suggest a relevant program coordinated by SOCS3 in different cell populations, devoted to the control of immune homeostasis in physiological and pathological conditions such as infection and autoimmunity.
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“HDAC5 promotes the upregulation of Chemokine ligand 2 (CCL2) by inhibiting SOCS3, thereby recruiting CCR2+ macrophages [147].”
From Targeting KRAS mutant cancers: from druggable therapy to drug resistance (2022) · cites this paper as [147]
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1 retracted
RETRACTED: Suppressors of Cytokine Signaling 2 and 3 Diametrically Control Macrophage Polarization
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RetractedYaşlı Kadınlarda Üreme Sağlığı
Kokanalı, D., & Engin Üstün, Y. (n.d.) · DergiPark (Istanbul University) · Cited by 170,090
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“Binding to the cytokine activates the kinase function of JAK, a tyrosine kinase that binds to the receptor, which auto-phosphorylates itself, cross-phosphorylates a JAK molecule bound to the accompanying heterodimer chain of the cytokine receptor and also different tyrosine sites on the cytokine receptor (1).”
BackgroundNotch Signaling: Cell Fate Control and Signal Integration in Development
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Leptin and the regulation of body weight in mammals
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“SOCS3 has been also suggested to inhibit IL-12-induced STAT4 activation by direct binding to IL-12Rβ2 (37), the IL-12R subunit that is not shared with the IL-23R.”
BackgroundInfluentialJournal of Biological Chemistry
Kurkinensp, M., CondongT, M. R., Blumberg, B., Barlow, D. P., Quiñones, S., Sausg, J., & Pihlajaniemisyy, T. (2021) · Journal of Biological Chemistry · doi:10.1074/jbc · Cited by 3,427
STATs: transcriptional control and biological impact
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Cited by
Sorted by citations
Li, L., Yu, R., Cai, T., Chen, Z., Lan, M., Zou, T., Wang, B., Wang, Q., Zhao, Y., & Cai, Y. (2020) · International Immunopharmacology · doi:10.1016/j.intimp.2020.106939 · Cited by 397
Macrophage and Fibroblast Interactions in Biomaterial‐Mediated Fibrosis
Witherel, C. E., Abebayehu, D., Barker, T. H., & Spiller, K. L. (2019) · Advanced Healthcare Materials · doi:10.1002/adhm.201801451 · Cited by 374
DNA methylation signatures of chronic low-grade inflammation are associated with complex diseases
WHI-EMPC Investigators, Ligthart, S., Disease, C. E. O. C. H., Marzi, C., Aslibekyan, S. W., Mendelson, M., Conneely, K. N., Tanaka, T., Colicino, E., Waite, L. L., et al. (2016) · Genome biology · doi:10.1186/s13059-016-1119-5 · Cited by 317
“The gene product of SOCS3, suppressor of cytokine signaling 3, plays a pivotal role in the innate immune system as a regulator of cytokine signaling [11].”
BackgroundT cell exhaustion during persistent viral infections
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Single‐cell transcriptomics reveals distinct inflammation‐induced microglia signatures
Sousa, C., Golebiewska, A., Poovathingal, S. K., Kaoma, T., Pires‐Afonso, Y., Martina, S., Coowar, D., Azuaje, F., Skupin, A., Balling, R., et al. (2018) · The EMBO Reports · doi:10.15252/embr.201846171 · Cited by 281
“Specifically, STAT3 and suppressor of cytokine signalling 3 (SOCS3) regulate inflammatory responses [54].”
Metadata
- Authors
- Carow, B., & Rottenberg, M. E.
- Affiliations
- Karolinska Institutet (SE)
- Corresponding author
- Carow, Berit
- ORCID
- Carow, Berit
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2014
- Volume
- 5
- Pages
- 58-58
- ISSN
- 1664-3224 (ISSN-L)
- PMC
- PMC3928676
- OpenAlex
- W2140013858
- Cited by
- 555
- References
- 179
- Citations by year
- 2026: 31 · 2025: 55 · 2024: 65 · 2023: 71 · 2022: 64 · 2021: 58 · 2020: 43 · 2019: 52 · 2018: 31 · 2017: 25 · 2016: 27 · 2015: 24 · 2014: 9
- FWCI
- 3.22
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Immunology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Keywords
- SOCS3, suppressor of cytokine signaling, infection, inflammation, autoimmune disease, STAT3 activation, JAK kinases, cytokine signaling, receptor ubiquitination, proteasomal degradation, immune homeostasis, myeloid cells, lymphoid cells
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