The DOI matches its Crossref record; 85 of the 85 references it cites were found in a registry or an index.
Regulation of nuclear factor-κB in autoimmunity
Open accessAbstract
NF-κB transcription factors are pivotal regulators of innate and adaptive immune responses, and perturbations of NF-κB signaling contribute to the pathogenesis of immunological disorders. NF-κB is a well-known proinflammatory mediator, and its deregulated activation is associated with the chronic inflammation of autoimmune diseases. Paradoxically, NF-κB plays a crucial role in the establishment of immune tolerance, including both central tolerance and the peripheral function of regulatory T (Treg) cells. Thus, defect or deregulated activation of NF-κB may contribute to autoimmunity and inflammation, highlighting the importance of tightly controlled NF-κB signaling. This review will focus on the recent progress regarding NF-κB regulation and its association with autoimmunity.
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Cites
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NF-κB signaling in inflammation
Liu, T., Zhang, L., Joo, D., & Sun, S.-C. (2017) · Signal Transduction and Targeted Therapy · doi:10.1038/sigtrans.2017.23 · Cited by 8,791
Self-citationNF‐κB signaling in inflammation and cancer
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Physiology of the Endometrium and Regulation of Menstruation
Critchley, H. O. D., Maybin, J. A., Armstrong, G. M., & Williams, A. R. W. (2020) · Physiological Reviews · doi:10.1152/physrev.00031.2019 · Cited by 536
NF-κB in inflammation and cancer
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Self-citationNF-κB in inflammation and renal diseases
Zhang, H., & Sun, S.-C. (2015) · Cell & Bioscience · doi:10.1186/s13578-015-0056-4 · Cited by 383
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Metadata
- Authors
- Sun, S.-C., Chang, J.-H., & Jin, J.
- Venue
- Trends in Immunology
- Publisher
- Elsevier BV
- Published
- 2013-06
- Volume
- 34
- Issue
- 6
- Pages
- 282-289
- ISSN
- 1471-4906 (ISSN-L)
- OpenAlex
- W2042233123
- Cited by
- 321
- References
- 85
- FWCI
- 1.04
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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