ArticleEuropean journal of immunology2008
CD40 ligation decreases its protein half-life at the cell surface.
Article in European journal of immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Synergy and antagonism in the integration of BCR and CD40 signals that control B-cell population expansion.Molecular systems biology · 2025Article
- CAR T cell-induced cytokine release syndrome is mediated by macrophages and abated by IL-1 blockade.Nature medicine · 2018Article
- Regulation of fibroblast growth factor-inducible 14 (Fn14) expression levels via ligand-independent lysosomal degradation.The Journal of biological chemistry · 2014Article
- Inter-α-inhibitor blocks epithelial sodium channel activation and decreases nasal potential differences in ΔF508 mice.American journal of respiratory cell and molecular biology · 2014Article
- Epithelial cells as immune effector cells: the role of CD40.Seminars in immunology · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
CD40 is expressed on a variety of tumors; anti-CD40 agonists promote tumor cell apoptosis and subsequent tumor regression. Because the effectiveness of anti-CD40- agonists is dependent upon CD40 surface expression, the current study examined ligation-mediated changes in CD40 protein half-life (t(1/2))( )at the cell surface. This study utilized a CD40(+) epithelial cell line (9HTEo-), a CD40 null epithelial cell line (HT-29) engineered to express either wild-type (WT) or mutant (T254A, Q263A, E235A, Delta201) CD40, and the anti-CD40 antibody G28.5. Ligation of endogenous CD40 expressed on 9HTEo- cells decreased CD40 surface protein t(1/2 )from 13 to 4 h (p <0.05). Ligation of WT-, Q263A-, or T254A-CD40 expressed on engineered HT-29 cells decreased CD40 surface protein t(1/2) from an average of 8 to 4 h (p <0.05); T254A and Q263A contain mutated TNF receptor-associated factor (TRAF)2/3-binding sites. In contrast, ligation of E235A and Delta201-CD40 had no affect on its surface protein t(1/2) (p <0.05); E235A contains a mutated TRAF6-binding site while Delta201 lacks an intact cytoplasmic tail. These results suggest that anti-CD40 agonists decrease CD40 surface protein t(1/2) via a mechanism that involves TRAF6 but not TRAF2/3. The therapeutic implications for CD40-mediated tumor regression are discussed.
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What OpenQuestion holds
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.