ArticleMolecular and cellular biology2014
HuR regulates alternative splicing of the TRA2β gene in human colon cancer cells under oxidative stress.
Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 69 citations in OpenAlex.
- Article
- Transcriptome-wide splicing analysis reveals HuR-regulated post-transcriptional programs in osteocytes.iScience · 2026Article
- SpliceSelectNet: a hierarchical Transformer-based deep learning model for splice site prediction.Nucleic acids research · 2026Article
- Review
- Proteomic Profiling of Human Extracellular Vesicles Reveals Diagnostic Biomarkers for Colon Adenocarcinoma.Journal of extracellular vesicles · 2026Article
- ELAV/Hu RNA-binding protein family: key regulators in neurological disorders, cancer, and other diseases.RNA biology · 2025Review
- Single-molecule imaging of transcription dynamics, RNA localization and fate in human T cells.The EMBO journal · 2025Article
- The potential impact of RNA splicing abnormalities on immune regulation in endometrial cancer.Cell death & disease · 2025Review
- Post-transcriptional regulation by HuR in colorectal cancer: impacts on tumor progression and therapeutic strategies.Frontiers in immunology · 2025Review
- HuR controls glutaminase RNA metabolism.Nature communications · 2024Article
- CircNUP54 promotes hepatocellular carcinoma progression via facilitating HuR cytoplasmic export and stabilizing BIRC3 mRNA.Cell death & disease · 2024Article
- Identification of HuR-RNA Interfering Compounds by Dynamic Combinatorial Chemistry and Fluorescence Polarization.ACS medicinal chemistry letters · 2023Article
- Targeting the RNA-Binding Protein HuR in Cancer.Cancer research · 2023Review
- An AKT1-and TRIM21-mediated phosphodegron controls proteasomal degradation of HuR enabling cell survival under heat shock.iScience · 2023Article
- Stress-Inducible SCAND Factors Suppress the Stress Response and Are Biomarkers for Enhanced Prognosis in Cancers.International journal of molecular sciences · 2023Article
- Epigenomic reprogramming in iAs-mediated carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Review
- HuR-dependent SOD2 protein synthesis is an early adaptation to anchorage-independence.Redox biology · 2022Article
- Hu Antigen R (HuR) Protein Structure, Function and Regulation in Hepatobiliary Tumors.Cancers · 2022Review
- Research progress on RNA-binding proteins in breast cancer.Oncology letters · 2022Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hu antigen R (HuR) regulates stress responses through stabilizing and/or facilitating the translation of target mRNAs. The human TRA2β gene encodes splicing factor transformer 2β (Tra2β) and generates 5 mRNA isoforms (TRA2β1 to -5) through alternative splicing. Exposure of HCT116 colon cancer cells to sodium arsenite stimulated checkpoint kinase 2 (Chk2)- and mitogen-activated protein kinase p38 (p38(MAPK))-mediated phosphorylation of HuR at positions S88 and T118. This induced an association between HuR and the 39-nucleotide (nt) proximal region of TRA2β exon 2, generating a TRA2β4 mRNA that includes exon 2, which has multiple premature stop codons. HuR knockdown or Chk2/p38(MAPK) double knockdown inhibited the arsenite-stimulated production of TRA2β4 and increased Tra2β protein, facilitating Tra2β-dependent inclusion of exons in target pre-mRNAs. The effects of HuR knockdown or Chk2/p38(MAPK) double knockdown were also confirmed using a TRA2β minigene spanning exons 1 to 4, and the effects disappeared when the 39-nt region was deleted from the minigene. In endogenous HuR knockdown cells, the overexpression of a HuR mutant that could not be phosphorylated (with changes of serine to alanine at position 88 [S88A], S100A, and T118A) blocked the associated TRA2β4 interaction and TRA2β4 generation, while the overexpression of a phosphomimetic HuR (with mutations S88D, S100D, and T118D) restored the TRA2β4-related activities. Our findings revealed the potential role of nuclear HuR in the regulation of alternative splicing programs under oxidative stress.
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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.