ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Fas apoptosis inhibitory molecule expression in B cells is regulated through IRF4 in a feed-forward mechanism.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Early B cell transcriptomic markers of measles-specific humoral immunity following a 3Frontiers in immunology · 2024Article
- Newfound physiological function of FAIM protein offers hope of novel disease-modifying therapy for Alzheimer's disease.Neural regeneration research · 2023Article
- Small Heat Shock Proteins Collaborate with FAIM to Prevent Accumulation of Misfolded Protein Aggregates.International journal of molecular sciences · 2022Article
- In search of the Aplysia immunome: an in silico study.BMC genomics · 2022Article
- Interferon Regulatory Factor Family Genes: At the Crossroads between Immunity and Head and Neck Squamous Carcinoma.Disease markers · 2022Article
- Fas Apoptosis Inhibitory Molecule Blocks and Dissolves Pathological Amyloid-β Species.Frontiers in molecular neuroscience · 2021Article
- Article
- Neurodegeneration and neuroinflammation: two processes, one target.Neural regeneration research · 2015Article
- Amyloid-β reduces the expression of neuronal FAIM-L, thereby shifting the inflammatory response mediated by TNFα from neuronal protection to death.Cell death & disease · 2015Article
- Article
- Expression analysis, single nucleotide polymorphisms and combined genotypes in candidate genes and their associations with growth and carcass traits in Qinchuan cattle.Molecular biology reports · 2013Article
- IRF4 is a suppressor of c-Myc induced B cell leukemia.PloS one · 2011Article
- Crystallization and preliminary X-ray crystallographic studies of human FAIM protein.Acta crystallographica. Section F, Structural biology and crystallization communications · 2010Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Fas apoptosis inhibitory molecule (FAIM) was originally cloned as an inhibitor of Fas-mediated apoptosis in B cells that has been reported to affect multiple cell types. Recently, we found that FAIM enhances CD40L-mediated signal transduction, including induction of IFN regulatory factor (IRF)4, in vitro and augments plasma cell production in vivo. These results have keyed interest in the regulation of FAIM expression, about which little is known. Here, we show that Faim is regulated by IRF4. The Faim promoter contains three IRF binding sites, any two of which promote Faim expression. Faim promoter activity is lost following mutation of all three IRF binding sites, whereas activity of the full promoter is enhanced by concurrent expression of IRF4. In stimulated primary B cells, IRF4 expression precedes FAIM expression, IRF4 binds directly to the Faim promoter, and loss of IRF4 results in the failure of stimulated Faim up-regulation. Finally, FAIM is preferentially expressed in germinal center B cells. Taken together, these results indicate that FAIM expression is regulated through IRF4 and that this most likely occurs as part of germinal center formation. Because FAIM enhances CD40-induced IRF4 expression in B cells, these results suggest that induction of FAIM initiates a positive reinforcing (i.e., feed-forward) system in which IRF4 expression is both enhanced by FAIM and promotes FAIM expression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.