The DOI matches its Crossref record; 55 of the 55 references it cites were found in a registry or an index.
Distinct roles for the NF-κB1 (p50) and c-Rel transcription factors in inflammatory arthritis
Open accessAbstract
Rheumatoid arthritis (RA) is a complex disease, with contributions from systemic autoimmunity and local inflammation. Persistent synovial joint inflammation and invasive synovial pannus tissue lead to joint destruction. RA is characterized by the production of inflammatory mediators, many of which are regulated by the Rel/NF-kappaB transcription factors. Although an attractive target for therapeutic intervention in inflammatory diseases, Rel/NF-kappaB is involved in normal physiology, thus global inhibition could be harmful. An alternate approach is to identify and target the Rel/NF-kappaB subunits critical for components of disease. To assess this, mice with null mutations in c-rel or nfkb1 were used to examine directly the roles of c-Rel and p50 in models of acute and chronic inflammatory arthritis. We found c-Rel-deficient mice were resistant to collagen-induced arthritis but had a normal response in an acute, destructive arthritis model (methylated BSA/IL-1 induced arthritis) suggesting c-Rel is required for systemic but not local joint disease. In contrast, p50-deficient mice were refractory to induction of both the chronic and acute arthritis models, showing this subunit is essential for local joint inflammation and destruction. Our data suggest Rel/NF-kappaB subunits play distinct roles in the pathogenesis of inflammatory arthritis and may provide a rationale for more specific therapeutic blockade of Rel/NF-kappaB in RA.
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“Disruption of TFBS for c-Rel (member of NF-ĸB TF family, linked to CIA development, and lymphoid cell growth and development [86]) and Sp1 (involved in cellular processes including growth, differentiation and apoptosis)”
From The oncoprotein TBX3 is controlling severity in experimental arthritis (2019) · cites this paper as [86]
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THE NF-κB AND IκB PROTEINS: New Discoveries and Insights
Baldwin, A. S. (1996) · Annual Review of Immunology · doi:10.1146/annurev.immunol.14.1.649 · Cited by 5,882
Nuclear Factor-κB — A Pivotal Transcription Factor in Chronic Inflammatory Diseases
Barnes, P. J., & Karin, M. (1997) · New England Journal of Medicine · doi:10.1056/nejm199704103361506 · Cited by 4,622
ROLE OF CYTOKINES IN RHEUMATOID ARTHRITIS
Feldmann, M., Brennan, F. M., & Maini, R. N. (1996) · Annual Review of Immunology · doi:10.1146/annurev.immunol.14.1.397 · Cited by 2,507
Auphan, N., DiDonato, J. A., Rosette, C., Helmberg, A., & Karin, M. (1995) · Science · doi:10.1126/science.270.5234.286 · Cited by 2,390
Structure, Regulation and Function of NF-kappaB
Siebenlist, U. K., Franzoso, G., & Brown, K. D. (1994) · Annual Review of Cell Biology · doi:10.1146/annurev.cb.10.110194.002201 · Cited by 2,086
Embryonic lethality and liver degeneration in mice lacking the RelA component of NF-κB
Beg, A. A., Sha, W. C., Bronson, R. T., Ghosh, S., & Baltimore, D. (1995) · Nature · doi:10.1038/376167a0 · Cited by 1,828
Inhibition of NF-κB by Sodium Salicylate and Aspirin
Kopp, E. B., & Ghosh, S. (1994) · Science · doi:10.1126/science.8052854 · Cited by 1,744
Role of Transcriptional Activation of IκBα in Mediation of Immunosuppression by Glucocorticoids
Scheinman, R. I., Cogswell, P. C., Lofquist, A. K., & Baldwin, A. S. (1995) · Science · doi:10.1126/science.270.5234.283 · Cited by 1,676
Kelley, W. N. (1985) · Virtual Defense Library (Ministerio de Defensa) · Cited by 1,641
NF-κB: A lesson in family values
Thanos, D., & Maniatis, T. (1995) · Cell · doi:10.1016/0092-8674(95)90506-5 · Cited by 1,247
Research works printed but not linked: 1
- Müller-Ladner, 1997, Am J Pathol, 149, 1607
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NF-κB regulation in the immune system
Li, Q., & Verma, I. M. (2002) · Nature Reviews Immunology · doi:10.1038/nri910 · Cited by 4,007
Matrix Metalloproteinases: Role In Arthritis
Peter, S. B. (2006) · Frontiers in bioscience · doi:10.2741/1817 · Cited by 1,310
NOD2 is a negative regulator of Toll-like receptor 2–mediated T helper type 1 responses
Watanabe, T., Kitani, A., Murray, P. J., & Strober, W. (2004) · Nature Immunology · doi:10.1038/ni1092 · Cited by 864
Vincenti, M. P., & Brinckerhoff, C. E. (2002) · Arthritis Research & Therapy · doi:10.1186/ar401 · Cited by 796
Functions of NF-κB1 and NF-κB2 in immune cell biology
Beinke, S., & Ley, S. C. (2004) · Biochemical Journal · doi:10.1042/bj20040544 · Cited by 611
Metadata
- Authors
- Campbell, I. K., Gerondakis, S., O’Donnell, K., & Wicks, I. P.
- Affiliations
- The Royal Melbourne Hospital (AU)
- Royal Prince Alfred Hospital (AU)
- Reid Health (US)
- Corresponding author
- Wicks, Ian P.
- Venue
- Journal of Clinical Investigation
- Published
- 2000-06-15
- Volume
- 105
- Issue
- 12
- Pages
- 1799-1806
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC378503
- OpenAlex
- W2042166751
- Cited by
- 168
- References
- 55
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 7 · 2023: 2 · 2022: 1 · 2021: 2 · 2020: 7 · 2019: 3 · 2018: 3 · 2017: 2 · 2016: 6 · 2015: 3 · 2014: 2 · 2013: 3 · 2012: 11
- FWCI
- 4.89
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Arthritis Foundation
- California Institute of Technology
- Arthritis Foundation of Australia
- Medical Research Council
- National Health and Medical Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Health Sciences › Medicine › Complementary and alternative medicine › Natural Compounds in Disease Treatment
- Keywords
- rheumatoid arthritis, c-Rel, collagen-induced arthritis, synovitis, joint destruction, pannus formation, arthritis pathogenesis
- MeSH terms
- Acute Disease, Animals, Arthritis, Experimental, Chronic Disease, Collagen, Crosses, Genetic, Inflammation, Joints, Mice, Inbred C57BL, Transcription Factors, NF-kappa B, Mice, Knockout, Proto-Oncogene Proteins c-rel, Genes, rel, Mice, NF-kappa B p50 Subunit
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