Trial reportJournal of immunology (Baltimore, Md. : 1950)2004
A novel mechanism of alternative promoter and splicing regulates the epitope generation of tumor antigen CML66-L.
Trial report in Journal of immunology (Baltimore, Md. : 1950), 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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
24 citing papers in PubMed.
- Reduced R-loop abundance at proinflammatory loci: a shared epigenetic mechanism in inflammatory and metabolic diseases.Frontiers in cardiovascular medicine · 2026Article
- Discovery of Seven ROS-Sensitive Immune Checkpoints and 46 Ligands Mediating Immune Suppression Through T cell-APC Networks.Journal of Cancer · 2026Article
- Novel NUDCD1 gene variant predisposes to severe COVID-19 disease in Asians through modulation of antiviral DHX15- and MAVS-mediated signalling.Frontiers in immunology · 2025Article
- Immune Checkpoints Are New Therapeutic Targets in Regulating Cardio-, and Cerebro-Vascular Diseases and CD4International journal of drug discovery and pharmacology · 2024Article
- Protein-rich foods, sea foods, and gut microbiota amplify immune responses in chronic diseases and cancers - Targeting PERK as a novel therapeutic strategy for chronic inflammatory diseases, neurodegenerative disorders, and cancer.Pharmacology & therapeutics · 2024Review
- Cigarette Smoke and Morphine Promote Treg Plasticity to Th17 via Enhancing Trained Immunity.Cells · 2022Article
- The immune landscape in BCR-ABL negative myeloproliferative neoplasms: inflammation, infections and opportunities for immunotherapy.British journal of haematology · 2022Review
- Article
- Canonical Secretomes, Innate Immune Caspase-1-, 4/11-Gasdermin D Non-Canonical Secretomes and Exosomes May Contribute to Maintain Treg-Ness for Treg Immunosuppression, Tissue Repair and Modulate Anti-Tumor ImmunityFrontiers in immunology · 2021Article
- Increasing Upstream Chromatin Long-Range Interactions May Favor Induction of Circular RNAs in LysoPC-Activated Human Aortic Endothelial Cells.Frontiers in physiology · 2019Article
- NUDCD1 promotes metastasis through inducing EMT and inhibiting apoptosis in colorectal cancer.American journal of cancer research · 2018Article
- Protein interaction network of alternatively spliced NudCD1 isoforms.Scientific reports · 2017Article
- High expression and frequently humoral immune response of melanoma-associated antigen D4 in glioma.International journal of clinical and experimental pathology · 2014Article
- Systematic analysis of protein pools, isoforms, and modifications affecting turnover and subcellular localization.Molecular & cellular proteomics : MCP · 2012Article
- Inflammatory and autoimmune reactions in atherosclerosis and vaccine design informatics.Journal of biomedicine & biotechnology · 2010Review
- Applications of RNA interference in cancer therapeutics as a powerful tool for suppressing gene expression.Molecular biology reports · 2009Review
- Article
- Novel tumor antigens elicit anti-tumor humoral immune reactions in a subset of patients with polycythemia vera.Clinical immunology (Orlando, Fla.) · 2007Article
- An unconventional antigen translated by a novel internal ribosome entry site elicits antitumor humoral immune reactions.Journal of immunology (Baltimore, Md. : 1950) · 2006Article
- Alternative splicing factor ASF/SF2 is down regulated in inflamed muscle.Journal of clinical pathology · 2006Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
This report describes the difference in the epitope generation of two isoforms of self-tumor Ag CML66 and the regulation mechanism. We identified a new CML66 short isoform, termed CML66-S. The previously identified long CML66 is referred to as CML66-L. CML66-S shares the C terminus with CML66-L but has its unique N terminus. CML66-S is predominantly expressed in testis, but is also expressed in very low levels in tumor cells, whereas CML66-L is expressed in tumor cells and testis. Differential expression of CML66-L and CML66-S in tumor cells resulted from regulation at transcription, although alternative splicing also participated in the generation of the isoforms. In addition, Ab titers to a CML66-L peptide were significantly higher than that to CML66-S peptide in the sera from patients with tumors. Finally, the Abs to full-length CML66-L in the sera from patients with tumors were correlated with the Abs in the sera from these patients to CML66-L-38, which is a fusion protein with a CML66-L-specific N terminus. This suggests that the CML66-L isoform is mainly responsible for the epitope generation. Our studies have identified the alternative promoter in combination with alternative splicing as a novel mechanism for regulation of the epitope generation of a self-tumor Ag.
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