ArticleJournal of neuroimmunology2016
Isoaspartylation appears to trigger small cell lung cancer-associated autoimmunity against neuronal protein ELAVL4.
Article in Journal of neuroimmunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- CKG-TPI: integrating collaborative knowledge graph with sequence interactions for TCR-peptide binding specificity.Briefings in bioinformatics · 2025Article
- Mechanisms of autoimmune-mediated paraneoplastic syndromes: immune tolerance and disease pathogenesis.Frontiers in immunology · 2025Review
- Breaking tolerance: autoantibodies can target protein posttranslational modifications.Current opinion in biotechnology · 2024Review
- Posttranslational modifications induce autoantibodies with risk prediction capability in patients with small cell lung cancer.Science translational medicine · 2023Article
- Data on isoaspartylation of neuronal ELAVL proteins.Data in brief · 2016Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
Autoantibodies against SCLC-associated neuronal antigen ELAVL4 (HuD) have been linked to smaller tumors and improved survival, but the antigenic epitope and mechanism of autoimmunity have never been solved. We report that recombinant human ELAVL4 protein incubated under physiological conditions acquires isoaspartylation, a type of immunogenic protein damage. Specifically, the N-terminal region of ELAVL4, previously implicated in SCLC-associated autoimmunity, undergoes isoaspartylation in vitro, is recognized by sera from anti-ELAVL4 positive SCLC patients and is highly immunogenic in subcutaneously injected mice and in vitro stimulated human lymphocytes. Our data suggest that isoaspartylated ELAVL4 is the trigger for the SCLC-associated anti-ELAVL4 autoimmune response.
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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.