ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
SSR4 Sustains Tertiary Lymphoid Structures by Regulation Quality Control of N-linked Glycosylation During B-cell Differentiation Into Plasmacyte in Colorectal Cancer.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
16 authors.
Funding
Abstract
Intratumoral tertiary lymphoid structure (TLS) fosters B-cell differentiation and antibody production, yet the intrinsic programs sustaining these functions remain unclear. By integrating spatial transcriptomics and single-cell RNA sequencing of colorectal cancer, we delineate a B-cell trajectory enriched for endoplasmic reticulum protein processing, autophagy, NF-κB signaling, and N-linked glycosylation, highlighting SSR4 as a progressively induced TRAP-complex component. SSR4 is further upregulated in B cells from anti-PD-1 responders. B-cell-specific Ssr4 deletion leads to peripheral B-cell loss, reduced antibody output, exacerbated colitis, and impaired mucosal immunity. Mechanistically, SSR4 interacts with DDOST to regulate BAFFR N-glycosylation, thereby sustaining B-cell activation and LTα1β2 expression via NF-κB signaling. In Apc
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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.