ArticleNature communications2017
Tia1 dependent regulation of mRNA subcellular location and translation controls p53 expression in B cells.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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Who cites it
49 citing papers in PubMed, 70 citations in OpenAlex.
- Review
- Review
- Targeting RNA binding proteins with small-molecule inhibitors: Advances, challenges, and therapeutic opportunities.Acta pharmaceutica Sinica. B · 2026Review
- Expression Patterns of T-Cell Intracellular Antigen 1 in Neurodegenerative Disorders and Stroke.International journal of molecular sciences · 2026Review
- Annexin A7 enhances TIA1 axonal trafficking to counteract pathological aggregation in neurons.The EMBO journal · 2025Article
- Structural basis for T-cell intracellular antigen-1 amyloid fibril formation revealed by cryo-electron microscopy.PNAS nexus · 2025Article
- Posttranscriptional control of the B cell receptor by HuR is essential for innate B cell maintenance and function.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Biomolecular condensates in immune cell fate.Nature reviews. Immunology · 2025Review
- TP53 minigene analysis of 161 sequence changes provides evidence for role of spatial constraint and regulatory elements on variant-induced splicing impact.NPJ genomic medicine · 2025Article
- Review
- FAK and p130Cas Modulate Stiffness-Mediated Early Transcription and Cellular Metabolism.Cytoskeleton (Hoboken, N.J.) · 2025Article
- A Computational Recognition Analysis of Promising Prognostic Biomarkers in Breast, Colon and Lung Cancer Patients.International journal of molecular sciences · 2025Article
- From regulation to deregulation of p53 in hematologic malignancies: implications for diagnosis, prognosis and therapy.Biomarker research · 2024Review
- Review
- Understanding the complexity of p53 in a new era of tumor suppression.Cancer cell · 2024Review
- FAK and p130Cas modulate stiffness-mediated early transcription and cellular metabolism.bioRxiv : the preprint server for biology · 2024Article
- Multiple roles for AU-rich RNA binding proteins in the development of haematologic malignancies and their resistance to chemotherapy.RNA biology · 2024Review
- The RNA binding proteins TIA1 and TIAL1 promote Mcl1 mRNA translation to protect germinal center responses from apoptosis.Cellular & molecular immunology · 2023Article
- Surmounting Cancer Drug Resistance: New Perspective on RNA-Binding Proteins.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Translocation of cytosolic human Cdc73 to stress granules plays a role in arsenic stress-induced stabilization of p53 mRNA.Journal of cell science · 2023Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
Post-transcriptional regulation of cellular mRNA is essential for protein synthesis. Here we describe the importance of mRNA translational repression and mRNA subcellular location for protein expression during B lymphocyte activation and the DNA damage response. Cytoplasmic RNA granules are formed upon cell activation with mitogens, including stress granules that contain the RNA binding protein Tia1. Tia1 binds to a subset of transcripts involved in cell stress, including p53 mRNA, and controls translational silencing and RNA granule localization. DNA damage promotes mRNA relocation and translation in part due to dissociation of Tia1 from its mRNA targets. Upon DNA damage, p53 mRNA is released from stress granules and associates with polyribosomes to increase protein synthesis in a CAP-independent manner. Global analysis of cellular mRNA abundance and translation indicates that this is an extended ATM-dependent mechanism to increase protein expression of key modulators of the DNA damage response.Sequestering mRNA in cytoplasmic stress granules is a mechanism for translational repression. Here the authors find that p53 mRNA, present in stress granules in activated B lymphocytes, is released upon DNA damage and is translated in a CAP-independent manner.
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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.