ArticleExperimental cell research2013
CEACAM1 regulates Fas-mediated apoptosis in Jurkat T-cells via its interaction with β-catenin.
Article in Experimental cell research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- TIM-3+ Macrophages: Insights into Their Role in Cancer and Inflammation.International journal of molecular sciences · 2026Review
- Structural aspects of CEACAM1 interactions.European journal of clinical investigation · 2024Review
- Regulation of lipid storage and inflammation in the liver by CEACAM1.European journal of clinical investigation · 2024Review
- Mechanism and function of CEACAM1 splice isoforms.European journal of clinical investigation · 2024Review
- High-dimensional mapping of human CEACAM1 expression on immune cells and association with melanoma drug resistance.Communications medicine · 2024Article
- The role of carcinoembryonic antigen-related cell adhesion molecule 1 in cancer.Frontiers in immunology · 2023Review
- TIM-3 drives temporal differences in restimulation-induced cell death sensitivity in effector CD8Cell death & disease · 2021Article
- A review of the relatively complex mechanism of JS-K induced apoptosis in cancer cells.Translational cancer research · 2019Review
- CEACAM1 structure and function in immunity and its therapeutic implications.Seminars in immunology · 2019Review
- Unaltered Fungal Burden and Lethality in Human CEACAM1-Transgenic Mice DuringFrontiers in microbiology · 2019Article
- CEACAM1 in Liver Injury, Metabolic and Immune Regulation.International journal of molecular sciences · 2018Review
- Effect of CEACAM-1 knockdown in human colorectal cancer cells.Oncology letters · 2018Article
- Abnormal expression of circulating and tumor-infiltrating carcinoembryonic antigen-related cell adhesion molecule 1 in patients with glioma.Oncology letters · 2018Article
- Not All Immune Checkpoints Are Created Equal.Frontiers in immunology · 2018Review
- Antioxidative CXXC Peptide Motif From Mesencephalic Astrocyte-Derived Neurotrophic Factor Antagonizes Programmed Cell Death.Frontiers in cell and developmental biology · 2018Article
- Article
- Induction of Lumen Formation in a Three-dimensional Model of Mammary Morphogenesis by Transcriptional Regulator ID4: ROLE OF CaMK2D IN THE EPIGENETIC REGULATION OF ID4 GENE EXPRESSION.The Journal of biological chemistry · 2016Article
- Loss of CEACAM1, a Tumor-Associated Factor, Attenuates Post-infarction Cardiac Remodeling by Inhibiting Apoptosis.Scientific reports · 2016Article
- CEACAM1 promotes melanoma cell growth through Sox-2.Neoplasia (New York, N.Y.) · 2014Article
- Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
CEACAM1 (Carcinoembryonic Antigen Cell Adhesion molecule 1), an activation induced cell surface marker of T-cells, modulates the T-cell immune response by inhibition of the T-cell and IL-2 receptors. Since T-cells undergo activation induced cell death via Fas activation, it was of interest to determine if this pathway was also affected by CEACAM1. Previously, we identified a novel biochemical interaction between CEACAM1 and the armadillo repeats of β-catenin in Jurkat cells, in which two critical residues, H469 and K470 of the cytoplasmic domain of CEACAM1-4L played an essential role; while in other studies, β-catenin was shown to regulate Fas-mediated apoptosis in Jurkat cells. CEACAM1 expression in Jurkat cells leads to the re-distribution of β-catenin to the actin cytoskeleton as well as inhibition of β-catenin tyrosine phosphorylation and its degradation after Fas stimulation. As a result, Fas-mediated apoptosis in these cells was inhibited. The K470A mutation of CEACAM1 partially rescued the inhibitory effect, in agreement with the prediction that a CEACAM1-β-catenin interaction pathway is involved. Although CEACAM1 has two ITIMs, they were not tyrosine-phosphorylated upon Fas ligation, indicating an ITIM independent mechanism; however, mutation of the critical residue S508, located between the ITIMs, to aspartic acid and a prerequisite for ITIM activation, abrogates the inhibitory activity of CEACAM1 to Fas-mediated apoptosis. Since Fas-mediated apoptosis is a major form of activation-induced cell death, our finding supports the idea that CEACAM1 is a general inhibitory molecule for T-cell activation utilizing a variety of pathways.
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