ArticleNature communications2025
The sex-biased chromatin modifier SMC1A promotes autoimmunity by shaping inflammatory pathways in patients with SLE.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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1 citing paper in PubMed.
- Escape from X-chromosome inactivation: from gene discovery to regulatory mechanisms.Biochemical Society transactions · 2026Review
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15 authors.
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Abstract
A strong female bias is characteristic of systemic lupus erythematosus (SLE), the prototypic systemic autoimmune disease. Here, through an unbiased transcriptome analysis, we report a pronounced female-biased expression of the cohesin complex subunit SMC1A, a genome architectural factor, in monocytes from SLE patients compared to those from healthy individuals or patients with ankylosing spondylitis, a non-sex-biased autoimmune disorder. Integration of SMC1A binding, chromatin activity, and accessibility in lupus-like monocytes reveals extensive SMC1A redistribution to active enhancers of immune/inflammatory genes, inducing their transcription. SLE monocyte transcriptomes demonstrate significant enrichment of female-biased immune/inflammatory genes among SMC1A targets, accompanied by increased secretion of cytokines including IL6, with enhanced SMC1A binding at their enhancers in lupus-like monocytes. Collectively, our study highlights SMC1A as a female-biased chromatin modifier that acquires a specific regulatory function during lupus, accentuating inflammatory pathways and providing mechanistic insights into the female-biased predisposition to SLE and other autoimmune diseases.
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