ArticleThe EMBO journal1994
Two distinct mechanisms contribute to the constitutive activation of RelB in lymphoid cells.
Article in The EMBO journal, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 89 citations in OpenAlex.
- RelB and Neuroinflammation.Cells · 2021Review
- Biological characteristics of transcription factor RelB in different immune cell types: implications for the treatment of multiple sclerosis.Molecular brain · 2019Review
- Decreased expression of the NF-κB family member RelB in lung fibroblasts from Smokers with and without COPD potentiates cigarette smoke-induced COX-2 expression.Respiratory research · 2015Article
- Regulation of signal transduction by spatial parameters: a case in NF-κB oscillation.IET systems biology · 2015Article
- Evidence for active antigen presentation by monocyte/macrophages in response to stimulation with particles: the expression of NFκB transcription factors and costimulatory molecules.Inflammopharmacology · 2013Article
- Control of RelB during dendritic cell activation integrates canonical and noncanonical NF-κB pathways.Nature immunology · 2012Article
- Celebrating 25 years of NF-κB research.Immunological reviews · 2012Article
- Differential utilization of NF-kappaB RELA and RELB in response to extracellular versus intracellular polyIC stimulation in HT1080 cells.BMC immunology · 2011Article
- Nuclear factor-kappa B family member RelB inhibits human immunodeficiency virus-1 Tat-induced tumor necrosis factor-alpha production.PloS one · 2010Article
- Glutamate-induced NFkappaB activation in the retina.Investigative ophthalmology & visual science · 2009Article
- RelB is differentially regulated by IkappaB Kinase-alpha in B cells and mouse lung by cigarette smoke.American journal of respiratory cell and molecular biology · 2009Article
- Stabilization of RelB requires multidomain interactions with p100/p52.The Journal of biological chemistry · 2008Article
- Regulation of RelB expression during the initiation of dendritic cell differentiation.Molecular and cellular biology · 2005Article
- NIK-dependent RelB activation defines a unique signaling pathway for the development of V alpha 14i NKT cells.The Journal of experimental medicine · 2003Article
- RelB is required for Peyer's patch development: differential regulation of p52-RelB by lymphotoxin and TNF.The EMBO journal · 2003Article
- Transcription of the RelB gene is regulated by NF-kappaB.Oncogene · 2001Article
- RelB nuclear translocation regulates B cell MHC molecule, CD40 expression, and antigen-presenting cell function.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Up-regulation of BOB.1/OBF.1 expression in normal germinal center B cells and germinal center-derived lymphomas.The American journal of pathology · 2000Article
- RelB modulation of IkappaBalpha stability as a mechanism of transcription suppression of interleukin-1alpha (IL-1alpha), IL-1beta, and tumor necrosis factor alpha in fibroblasts.Molecular and cellular biology · 1999Article
- Expression of the RelB transcription factor correlates with the activation of human dendritic cells.Immunology · 1999Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The kappa B-motif is an important regulatory element both for constitutive lymphoid-specific as well as ubiquitous inducible transcriptional activity. We have shown previously that different members of the NF-kappa B/Rel family of transcription factors are responsible for these distinct functions. Whereas the p65/RelA protein is involved in inducible kappa B-dependent transcription, RelB is associated with constitutive activity in lymphoid cells. Here we have addressed the question of how RelB is constitutively activated in lymphoid cells. We demonstrate that this is achieved by two different mechanisms. Expression of relB as determined by measurement of stable RNA and protein levels is significantly enhanced in lymphoid organs compared with non-lymphoid organs. However, these observed differences in absolute amounts of RNA and protein would not suffice to explain the dramatic differences that are apparent at the level of active DNA binding complexes in extracts from the respective organs. We have therefore analyzed the interaction of RelB complexes with the I kappa B-alpha inhibitor protein. Our results show that RelB-containing complexes present in lymphoid extracts are much less susceptible to inhibition by I kappa B-alpha than RelA- or RelB-containing complexes from non-lymphoid cells. This difference might be due to post-translational modifications of the RelB protein or interaction with a lymphoid-specific cofactor for RelB.
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