ArticleNucleic acids research2019
XAB2 depletion induces intron retention in POLR2A to impair global transcription and promote cellular senescence.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Exon junction complex and nuclear pore complex components preferentially govern the nuclear export of spliced lncRNAs.Cell death discovery · 2026Article
- LMO7-mediated POLR2A degradation promotes cellular senescence through the MDM4/p53/p21 axis.Cell death & disease · 2026Article
- Article
- Splicing factor FUS facilitates the progression of PIT1-lineage PitNETs by upregulating MDM2.Theranostics · 2026Article
- Nuclear PD-L1 drives IFN-γ-promoted lung metastasis of triple-negative breast cancer via POLR2A-mediated transcriptional activation of LY6E.Breast cancer research : BCR · 2025Article
- USP10 Inhibits Ferroptosis via Deubiquinating POLR2A in Head and Neck Squamous Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Intron Retention: A Reemerging Paradigm in RNA Biology and Post-Transcriptional Gene Regulation.Genes · 2025Review
- USP10/XAB2/ANXA2 axis promotes DNA damage repair to enhance chemoresistance to oxaliplatin in colorectal cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- A defective splicing machinery promotes senescence through MDM4 alternative splicing.Aging cell · 2024Article
- KHSRP ameliorates acute liver failure by regulating pre-mRNA splicing through its interaction with SF3B1.Cell death & disease · 2024Article
- C-IGF1R encoded by cIGF1R acts as a molecular switch to restrict mitophagy of drug-tolerant persister tumour cells in non-small cell lung cancer.Cell death and differentiation · 2023Article
- Investigation of targets and anticancer mechanisms of covalently acting natural products by functional proteomics.Acta pharmacologica Sinica · 2023Article
- The XPA Protein-Life under Precise Control.Cells · 2022Review
- The splicing factor SF3B4 drives proliferation and invasion in cervical cancer by regulating SPAG5.Cell death discovery · 2022Article
- Application of RNA subcellular fraction estimation method to explore RNA localization regulation.G3 (Bethesda, Md.) · 2022Article
- Targeting the splicing factor NONO inhibits GBM progression through GPX1 intron retention.Theranostics · 2022Article
- The splicing factor XAB2 interacts with ERCC1-XPF and XPG for R-loop processing.Nature communications · 2021Article
- Article
- POLR2A Promotes the Proliferation of Gastric Cancer Cells by Advancing the Overall Cell Cycle Progression.Frontiers in genetics · 2021Article
- Prevalent intron retention fine-tunes gene expression and contributes to cellular senescence.Aging cell · 2020Article
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
XAB2 is a multi-functional protein participating processes including transcription, splicing, DNA repair and mRNA export. Here, we report POLR2A, the largest catalytic subunit of RNA polymerase II, as a major target gene down-regulated after XAB2 depletion. XAB2 depletion led to severe splicing defects of POLR2A with significant intron retention. Such defects resulted in substantial loss of POLR2A at RNA and protein levels, which further impaired global transcription. Treatment of splicing inhibitor madrasin induced similar reduction of POLR2A. Screen using TMT-based quantitative proteomics identified several proteins involved in mRNA surveillance including Dom34 with elevated expression. Inhibition of translation or depletion of Dom34 rescued the expression of POLR2A by stabilizing its mRNA. Immuno-precipitation further confirmed that XAB2 associated with spliceosome components important to POLR2A expression. Domain mapping revealed that TPR motifs 2-4 and 11 of XAB2 were critical for POLR2A expression by interacting with SNW1. Finally, we showed POLR2A mediated cell senescence caused by XAB2 deficiency. Depletion of XAB2 or POLR2A induced cell senescence by up-regulation of p53 and p21, re-expression of POLR2A after XAB2 depletion alleviated cellular senescence. These data together support that XAB2 serves as a guardian of POLR2A expression to ensure global gene expression and antagonize cell senescence.
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