RBM25 selectively stabilizes XBP1s mRNA independently of splicing factor activity

RBM25 selectively stabilizes spliced XBP1 mRNA during ER stress by binding the XBP1s 3' UTR and prolonging its half-life.

• Why it matters: The IRE1–XBP1 axis drives adaptive UPR, but how cells sustain XBP1s expression after splicing is not well defined.
• What they did: The study identifies RBM25 as an RNA-binding regulator that associates with the XBP1s 3' untranslated region, extending XBP1s mRNA half-life while leaving XBP1u and RIDD targets unchanged.
• The result: Depleting RBM25 reduces XBP1s-dependent transcriptional output, weakens adaptive UPR signaling, and increases sensitivity to ER stress–induced death across multiple stress paradigms.

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