Trial reportJournal of immunology (Baltimore, Md. : 1950)2013
Ro60 requires Y3 RNA for cell surface exposure and inflammation associated with cardiac manifestations of neonatal lupus.
Trial report in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 56 citations in OpenAlex.
- Hydroxychloroquine to Prevent Recurrent Congenital Heart Block in Fetuses of Anti-SSA/Ro-Positive Mothers.Journal of the American College of Cardiology · 2020Trial
- Monocyte surface Y RNAs potentiate innate immunity.Nature cell biology · 2026Article
- hY3 RNA binds and inhibits ribosomes and modulates the starvation-induced integrated stress response.Nucleic acids research · 2026Article
- RNY1 Is Heterogeneously Partitioned in Inflamed Airway Fluid and Modulates Pro-Inflammatory Macrophage Transcriptional Programming.Journal of extracellular biology · 2026Article
- Deciphering the RNA landscapes on mammalian cell surfaces.Protein & cell · 2026Article
- Glycosylated RNAs: discovery and implications in cancer biology.Frontiers in oncology · 2026Review
- RNY1 partitions into extracellular vesicles and ribonucleoprotein particles during airway inflammation to regulate macrophage programming.bioRxiv : the preprint server for biology · 2025Article
- Ro60-Roles in RNA Processing, Inflammation, and Rheumatic Autoimmune Diseases.International journal of molecular sciences · 2024Review
- PTBP1 protects Y RNA from cleavage leading to its apoptosis-specific degradation.Cell death discovery · 2024Article
- Biological basis of extensive pleiotropy between blood traits and cancer risk.Genome medicine · 2024Article
- Review
- Article
- IL-33/ST2 Activation Is involved in Ro60-Regulated Photosensitivity in Cutaneous Lupus Erythematosus.Mediators of inflammation · 2022Article
- Making Sense of Intracellular Nucleic Acid Sensing in Type I Interferon Activation in Sjögren's Syndrome.Journal of clinical medicine · 2021Review
- Noncoding Y RNAs regulate the levels, subcellular distribution and protein interactions of their Ro60 autoantigen partner.Nucleic acids research · 2020Article
- A guide to naming human non-coding RNA genes.The EMBO journal · 2020Review
- The Endogenous Plasma Small RNAome of Rheumatoid Arthritis.ACR open rheumatology · 2020Article
- Y RNAs: Biogenesis, Function and Implications for the Cardiovascular System.Advances in experimental medicine and biology · 2020Review
- Ro60 and Y RNAs: structure, functions, and roles in autoimmunity.Critical reviews in biochemistry and molecular biology · 2019Review
- Profiling of tRNA Halves and YRNA Fragments in Serum and Tissue From Oral Squamous Cell Carcinoma Patients Identify Key Role of 5' tRNA-Val-CAC-2-1 Half.Frontiers in oncology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiac neonatal lupus (NL) is presumed to arise from maternal autoantibody targeting an intracellular ribonucleoprotein, Ro60, which binds noncoding Y RNA and only becomes accessible to autoantibodies during apoptosis. Despite the importance of Ro60 trafficking in the development of cardiac NL, the mechanism underlying cell surface exposure is unknown. To evaluate the influence of Y RNA on the subcellular location of Ro60 during apoptosis and activation of macrophages, stable Ro60 knockout murine fibroblasts expressing wild-type or mutated FLAG-Ro60 were assessed. FLAG3-Ro60(K170A R174A) binds Y RNA, whereas FLAG3-Ro60(H187S) does not bind Y RNA; fibroblasts expressing these constructs showed equivalent intracellular expression of Ro60. In contrast, apoptotic fibroblasts containing FLAG3-Ro60(K170A R174A) were bound by anti-Ro60, whereas FLAG3-Ro60(H187S) was not surface expressed. RNA interference of mY3 RNA in wild-type fibroblasts inhibited surface translocation of Ro60 during apoptosis, whereas depletion of mY1 RNA did not affect Ro60 exposure. Furthermore, Ro60 was not exposed following overexpression of mY1 in the mY3-depleted fibroblasts. In an in vitro model of anti-Ro60-mediated injury, Y RNA was shown to be an obligate factor for TLR-dependent activation of macrophages challenged with anti-Ro60-opsonized apoptotic fibroblasts. Murine Y3 RNA is a necessary factor to support the surface translocation of Ro60, which is pivotal to the formation of immune complexes on apoptotic cells and a TLR-dependent proinflammatory cascade. Accordingly, the Y3 RNA moiety of the Ro60 ribonucleoprotein imparts a critical role in the pathogenicity of maternal anti-Ro60 autoantibodies.
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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.