The DOI matches its Crossref record; 94 of the 94 references it cites were found in a registry or an index.
Negative regulation of cytokine signaling
Abstract
Cytokines use complex signaling cascades to elicit their biological effects, many of which involve phosphorylation as a mechanism of activation. Rapid and efficient attenuation of cytokine signals is crucial to maintaining regulation of these processes and to preventing toxic side effects. Phosphatases have been shown to be involved in these regulatory processes, but more recent research has seen the discovery of two new families of negative regulators, the suppressor of cytokine signaling (SOCS) and protein inhibitors of signal transducer and activator of transcription (STAT) (PIAS) protein families. SOCS proteins are induced by and inhibit many cytokine-signaling systems in a classic negative-feedback loop, and the generation of transgenic and knockout models has greatly increased our understanding of their physiological functions. PIAS proteins interact with the transcriptional mediators of cytokine action, the STATs, to suppress their DNA-binding activity. These three classes of molecules form what is now emerging as an integrated system for deactivating cytokine signaling at a number of levels, from the receptor to the transcription factor.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Activation of cytokine signaling is coupled with multiple layers of negative regulation to ensure timely down-regulation of signaling, as exemplified by the SOCS system (17).”
From Gamma Interferon Triggers Interaction between ICSBP (IRF-8) and TEL, Recruiting the Histone Deacetylase HDAC3 to the Interferon-Responsive Element (2002) · cites this paper as [17]
Citations
Cites
A family of cytokine-inducible inhibitors of signalling
Starr, R., Willson, T. A., Viney, E. M., Murray, L. J. L., Rayner, J. R., Jenkins, B. J., Gonda, T. J., Alexander, W. S., Metcalf, D., Nicola, N. A., et al. (1997) · Nature · doi:10.1038/43206 · Cited by 2,066
Self-citationMoore, K. W., O’Garra, A., Malefyt, R. D. W., Vieira, P., & Mosmann, T. R. (1993) · Annual Review of Immunology · doi:10.1146/annurev.iy.11.040193.001121 · Cited by 1,883
Normal growth and development in the absence of hepatic insulin-like growth factor I
Yakar, S., Liu, J., STANNARD, B. S., Butler, A. A., Accili, D., Sauer, B., & LeRoith, D. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.13.7324 · Cited by 1,418
A new protein containing an SH2 domain that inhibits JAK kinases
Endo, T. A., Masuhara, M., Yokouchi, M., Suzuki, R., Sakamoto, H., Mitsui, K., Matsumoto, A., Tanimura, S., Ohtsubo, M., Misawa, H., et al. (1997) · Nature · doi:10.1038/43213 · Cited by 1,408
Teglund, S., McKay, C., Schuetz, E. G., van Deursen, J. M., Stravopodis, D. J., Wang, D., Brown, M. P., Bodner, S. M., Grosveld, G. C., & Ihle, J. N. (1998) · Cell · doi:10.1016/s0092-8674(00)81444-0 · Cited by 1,266
Stat5a is mandatory for adult mammary gland development and lactogenesis.
Liu, X., Robinson, G. W., Wagner, K. U., Garrett, L., Wynshaw-Boris, A., & Hennighausen, L. (1997) · Genes & Development · doi:10.1101/gad.11.2.179 · Cited by 1,111
Structure and function of a new STAT-induced STAT inhibitor
Naka, T., Narazaki, M., Hirata, M., Matsumoto, T., Minamoto, S., Aono, A., Nishimoto, N., Kajita, T., Taga, T., Yoshizaki, K., et al. (1997) · Nature · doi:10.1038/43219 · Cited by 1,040
Identification of SOCS-3 as a Potential Mediator of Central Leptin Resistance
Bjørbæk, C., Elmquist, J. K., Frantz, J. D., Shoelson, S. E., & Flier, J. S. (1998) · Molecular Cell · doi:10.1016/s1097-2765(00)80062-3 · Cited by 1,014
Requirement of STAT5b for sexual dimorphism of body growth rates and liver gene expression
Udy, G. B., Towers, R. P., Snell, R. G., Wilkins, R. J., Park, S.-H., Ram, P. A., Waxman, D. J., & Davey, H. W. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.14.7239 · Cited by 991
Specific Inhibition of Stat3 Signal Transduction by PIAS3
Chung, C. D., Liao, J., Liu, B., Rao, X., Jay, P., Berta, P., & Shuai, K. (1997) · Science · doi:10.1126/science.278.5344.1803 · Cited by 980
Flagged first, then by citations
Research works printed but not linked: 1
- Gresser, 1982, Can interferon induce diseasearticle-title, Interferon, 4, 95
Cited by
Sorted by citations
The JAK/STAT signaling pathway
Rawlings, J. S., Rosler, K. M., & Harrison, D. A. (2004) · Journal of Cell Science · doi:10.1242/jcs.00963 · Cited by 1,858
Regulation of JAK–STAT signalling in the immune system
Shuai, K., & Liu, B. (2003) · Nature reviews. Immunology · doi:10.1038/nri1226 · Cited by 1,410
Buettner, R., Mora, L. B., & Jove, R. (2002) · PubMed · Cited by 1,036
IL-6 and related cytokines as the critical lynchpins between inflammation and cancer
Taniguchi, K., & Karin, M. (2014) · Seminars in Immunology · doi:10.1016/j.smim.2014.01.001 · Cited by 724
Tuning the Cytokine Responses: An Update on Interleukin (IL)-4 and IL-13 Receptor Complexes
Junttila, I. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.00888 · Cited by 687
Metadata
- Authors
- Greenhalgh, C. J., & Hilton, D. J.
- Affiliations
- Walter and Eliza Hall Institute of Medical Research (AU)
- Corresponding author
- Greenhalgh, Christopher J
- ORCID
- Hilton, Douglas J
- Venue
- Journal of Leukocyte Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 2001-09-01
- Volume
- 70
- Issue
- 3
- Pages
- 348-356
- ISSN
- 0741-5400 (ISSN-L)
- 1938-3673
- OpenAlex
- W2107469094
- Cited by
- 258
- References
- 93
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 2 · 2022: 2 · 2021: 6 · 2020: 6 · 2019: 5 · 2018: 4 · 2017: 11 · 2016: 14 · 2015: 9 · 2014: 13 · 2013: 11 · 2012: 13
- FWCI
- 10.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Leukocyte Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Anti-Cancer Council of Victoria, Melbourne, Australia
- National Health and Medical Research Council, Canberra, Australia
- National Institutes of Health (CA-22556)
- Australian Federal Government Cooperative Research Centers Program
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- cytokine signaling, negative regulation, suppressor of cytokine signaling, STAT proteins, negative feedback loop, signal attenuation, protein phosphatase, transcriptional repression, DNA-binding activity
- MeSH terms
- Suppressor of Cytokine Signaling 1 Protein, Suppressor of Cytokine Signaling 3 Protein, Animals, Carrier Proteins, DNA-Binding Proteins, Models, Biological, Proteins, Repressor Proteins, Transcription Factors, Signal Transduction, Trans-Activators, Cytokines, Protein Tyrosine Phosphatases, Intracellular Signaling Peptides and Proteins, Suppressor of Cytokine Signaling Proteins, Protein Inhibitors of Activated STAT, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review