Evidence map›Paper›PMID 42411410›Full record

ArticleNucleic acids research2026

Neurochondrin promotes U5 snRNP maturation by regulating AAR2 release from PRPF8.

Tingrong Ren, Wanru Huang, Gaigai Wei, Haiping Zhao, Yuqi Zhang, Jingjing Yi, Zhihan Guo, Yihan Wang, Jiating Kuang, Zhaoying Sheng and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nucleic acids research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Tingrong RenFudan University Pudong Medical Center and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.ORCID 0000-0002-5415-7797
Wanru HuangFudan University Pudong Medical Center and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Gaigai WeiFudan University Pudong Medical Center and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Haiping ZhaoFudan University Pudong Medical Center and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Yuqi ZhangFudan University Pudong Medical Center and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Jingjing YiFudan University Pudong Medical Center and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Zhihan GuoFudan University Pudong Medical Center and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Yihan WangFudan University Pudong Medical Center and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Jiating KuangFudan University Pudong Medical Center and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Zhaoying ShengFudan University Pudong Medical Center and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.ORCID 0009-0009-2720-7101
Huiling ZhangFudan University Pudong Medical Center and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
Duanwu ZhangFudan University Pudong Medical Center and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism, Ministry of Science and Technology, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.ORCID 0000-0003-2946-846X

Funding

Fudan UniversityNational Natural Science Foundation of China 32370926National Natural Science Foundation of China 82071780Science and Technology Commission of Shanghai Municipality 21JC1400900
6 · The paper itself

Abstract

Pre-mRNA splicing is orchestrated by the spliceosome, a dynamic and highly regulated ribonucleoprotein complex composed of five small nuclear ribonucleoproteins (snRNPs). Despite extensive studies, the biogenesis of snRNPs remains incompletely understood. Here, we identify neurochondrin (NCDN) as a critical regulator of U5 snRNP biogenesis. NCDN associates with PRPF8-AAR2-EFTUD2 complex in the cytoplasm and is essential for the proper progression of this assembly intermediate toward mature U5 snRNP formation. Loss of NCDN causes the accumulation of this intermediate, resulting in a decreased level of mature U5 snRNP. Spliceosome dysregulation often leads to alternative splicing abnormalities implicated in cancer. Indeed, NCDN deficiency suppresses tumor cell proliferation and induces apoptosis, while high NCDN expression promotes tumor cell growth and correlates with poor survival in glioblastoma patients. Transcriptome analyses reveal that loss of NCDN causes widespread alternative splicing defects and changes in gene expression. Collectively, these results establish NCDN as an essential factor for U5 snRNP assembly and spliceosome function, and highlight its potential as a therapeutic target in glioma with elevated NCDN expression.

Indexed as

Nerve Tissue ProteinsRibonucleoprotein, U5 Small NuclearRNA-Binding ProteinsAlternative SplicingAnimalsCell Line, TumorCell ProliferationGlioblastomaHumansPeptide Elongation FactorsSpliceosomesEFTUD2 protein, humanNerve Tissue ProteinsPeptide Elongation FactorsPRPF8 protein, humanRibonucleoprotein, U5 Small NuclearRNA-Binding Proteins

Identifiers

PMID42411410
PMCPMC13338715

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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.