ArticleCellular and molecular life sciences : CMLS2025
The immune sensitivity caused by DUSP11, an RNA 5'-end maturation phosphatase, is adjusted by a human non-coding RNA, nc886.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- DUSP11 is an RNA triphosphatase that limits PspCas13b activity by destabilizing gRNA abundance in mammalian cells.Nucleic acids research · 2026Article
- DUSP11 is an Intracellular Innate Immune Checkpoint in Lung Adenocarcinoma.Cancer immunology research · 2025Article
- RNA Polymerase III-Transcribed RNAs in Health and Disease: Mechanisms, Dysfunction, and Future Directions.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors.
Funding
Abstract
All cellular transcripts initially have a tri-phosphate (PPP) group at the 5'-end, recognized as a pathogen-associated molecular pattern (PAMP) by a cell's innate immune system. The removal of 5'-PPP occurs to varying extents, causing immune imbalance. However, how cells manage this situation has not yet been documented. Among 5'-PPP removal mechanisms, recent attention has been towards an RNA phosphatase called Dual Specificity Phosphatase 11 (DUSP11), which acts preferentially on 5'-triphosphorylated (5'-PPP) RNAs transcribed by RNA polymerase III (Pol III) and converts them to a 5'-monophosphorylated (5'-P) form. Here we have elucidated that immune imbalance caused by variable DUSP11 expression in human is controlled by a Pol III-transcribed non-coding RNA (Pol III-ncRNA), nc886. DUSP11 depletion leads to the accumulation of 5'-PPP-Pol III-ncRNAs, making cells respond better to incoming PAMP. Distinctly from other Pol III-ncRNAs, DUSP11 depletion increases the expression of nc886 in a 5'-P form, which mitigates the sensitized immunity. nc886 expression is also increased by infection with Kaposi's sarcoma-associated herpesvirus (KSHV) that suppresses DUSP11, and, in turn, nc886 stimulates KSHV infectivity. DUSP11 levels in normal tissues are relatively constitutive in mice lacking nc886 but are variable in humans. This wide range of DUSP11 expression and the resultant immune imbalance is probably adjusted by nc886. In summary, our study of DUSP11 and nc886 has uncovered a novel mechanism by which human cells control immune sensitivity, which is intrinsically caused by cellular RNA metabolism, allowing different states of equilibrium between immune status and gene expression.
Indexed as
Identifiers
What Socratic 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 Socratic graph.