ReviewCells2019
New Frontiers: ARID3a in SLE.
Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 4 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
11 citing papers in PubMed, 4 syntheses or guidelines pooled it, 16 citations in OpenAlex.
- Genetic Architecture of Idiopathic Inflammatory Myopathies From Meta-Analyses.Arthritis & rheumatology (Hoboken, N.J.) · 2025Pooled it
- Exploration of common genomic signatures of systemic juvenile rheumatoid arthritis and type 1 diabetes.Scientific reports · 2023Pooled it
- A regulatory variant at 19p13.3 is associated with primary biliary cholangitis risk and ARID3A expression.Nature communications · 2023Pooled it
- Pooled it
- ARID3A Dysregulation Drives Colon Cancer Progression and Enhances Responsiveness to Aspirin.Journal of cellular and molecular medicine · 2026Article
- Plasma Exosomes Derived from Patients with Primary Immune Thrombocytopenia Attenuate TBX21Inflammation · 2025Article
- Unveiling the prognostic value of ARID3A in breast cancer through bioinformatic analysis.Heliyon · 2025Article
- ARID3a from the ARID family: structure, role in autoimmune diseases and drug discovery.Acta pharmacologica Sinica · 2023Review
- Missense Variants Reveal Functional Insights Into the Human ARID Family of Gene Regulators.Journal of molecular biology · 2022Article
- Deficiencies in the DNA Binding Protein ARID3a Alter Chromatin Structures Important for Early Human Erythropoiesis.ImmunoHorizons · 2021Article
- EpiRegio: analysis and retrieval of regulatory elements linked to genes.Nucleic acids research · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Systemic lupus erythematosus (SLE) is a devastating and heterogeneous autoimmune disease that affects multiple organs, and for which the underlying causes are unknown. The majority of SLE patients produce autoantibodies, have increased levels of type-I inflammatory cytokines, and can develop glomerulonephritis. Recent studies indicate an unexpected but strong association between increased disease activity in SLE patients and the expression of the DNA-binding protein ARID3a (A + T rich interaction domain protein 3a) in a number of peripheral blood cell types. ARID3a expression was first associated with autoantibody production in B cells; however, more recent findings also indicate associations with expression of the inflammatory cytokine interferon alpha in SLE plasmacytoid dendritic cells and low-density neutrophils. In addition, ARID3a is expressed in hematopoietic stem cells and some adult kidney progenitor cells. SLE cells expressing enhanced ARID3a levels show differential gene expression patterns compared with homologous healthy control cells, identifying new pathways potentially regulated by ARID3a. The associations of ARID3a expression with increased disease severity in SLE, suggest that it, or its downstream targets, may provide new therapeutic targets for SLE.
Indexed as
Identifiers
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.