ArticleMolecular and cellular biochemistry2021
Knockdown of RSAD2 attenuates B cell hyperactivity in patients with primary Sjögren's syndrome (pSS) via suppressing NF-κb signaling pathway.
Article in Molecular and cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Identification of a systemic lupus erythematosus disease signature in resting naive B cells.The Journal of clinical investigation · 2026Article
- Macrophage RSAD2 Couples mtDNA Synthesis With a Self-Amplifying Inflammatory Circuit to Orchestrate Tissue Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- AUF1 modulates cellular senescence in auditory hair cells by regulating the transcription and alternative splicing of immune response genes.Molecular biology reports · 2026Article
- Article
- Interferon-stimulated Viperin impairs Treg function in autoimmune thrombocytopenia.Cell communication and signaling : CCS · 2025Article
- Integrated study of DNA methylation and transcriptome: a new perspective for exploring the pathogenesis of Sjögren's syndrome.Epigenetics & chromatin · 2025Article
- Sjögren's Syndrome: Epidemiology, Classification Criteria, Molecular Pathogenesis, Diagnosis, and Treatment.MedComm · 2025Review
- Viperin: A Multifunctional Protein in Antiviral Immunity and Disease Pathogenesis.Pathogens (Basel, Switzerland) · 2025Review
- Crucial Roles of RSAD2/viperin in Immunomodulation, Mitochondrial Metabolism and Autoimmune Diseases.Inflammation · 2025Review
- Unveiling hub genes and biological pathways: A bioinformatics analysis of Trauma-Induced Coagulopathy (TIC).PloS one · 2025Article
- USP18-mediated protein stabilization of NOTCH1 is associated with altered Th17/Treg cell ratios and B cell-mediated autoantibody secretion in Sjögren syndrome.Immunologic research · 2024Article
- Transcriptomics explores potential mechanisms for the development of Primary Sjogren's syndrome to diffuse large B-cell lymphoma in B cells.BMC immunology · 2024Article
- PRMT5 participates in B cell overactivation in patients with primary Sjogren's syndrome (pSS) through RSAD2-mediated NF-κB signaling.Immunity, inflammation and disease · 2023Article
- The Spectrum of Extraglandular Manifestations in Primary Sjögren's Syndrome.Journal of personalized medicine · 2023Review
- Comprehensive analysis of gut microbiome and host transcriptome in chickens afterFrontiers in cellular and infection microbiology · 2023Article
- Exploring the shared molecular mechanisms between systemic lupus erythematosus and primary Sjögren's syndrome based on integrated bioinformatics and single-cell RNA-seq analysis.Frontiers in immunology · 2023Article
- Radical-SAM dependent nucleotide dehydratase (SAND), rectification of the names of an ancient iron-sulfur enzyme using NC-IUBMB recommendations.Frontiers in molecular biosciences · 2022Article
- Identification of key interferon-stimulated genes for indicating the condition of patients with systemic lupus erythematosus.Frontiers in immunology · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Primary Sjögren's syndrome (pSS) is a chronic autoimmune disease that is mainly characterized as abnormal activation of B cells. It is reported that radical s-adenosyl methionine domain-containing 2 (RSAD2) is overexpressed in CD19+ B cells of pSS patients, but its role in pSS B cells remains unknown. Herein, RSAD2 expression was upregulated in CD19+ B cells of pSS patients and positively correlated with the expression of interleukin-10 (IL-10) in serum. After CD40L stimulation, knockdown of RSAD2 significantly attenuated cell viability, the production levels of immunoglobins and the expression of IL-10, while promoted cell apoptosis of pSS CD19+ B cells. Mechanistically, knockdown of RSAD2 negatively regulated nuclear factor kappa-b (NF-κb) signaling pathway. In addition, overexpression of p65 prominently alleviated the inhibitory effect of RSAD2 knockdown on proliferation, immunoglobin production and IL-10 expression in CD40L-induced CD19+ B cells. Our study indicated that silencing RSAD2 attenuated pSS B cell hyperactivity via suppressing NF-κb signaling pathway, which might provide a potential therapeutic target for pSS treatment.
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