ArticleJournal of immunology (Baltimore, Md. : 1950)2015
B Cell-Intrinsic Expression of the HuR RNA-Binding Protein Is Required for the T Cell-Dependent Immune Response In Vivo.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- The Role of Tumor-Intrinsic HuR in Modeling the Pancreatic Tumor Microenvironment: Molecular Mechanisms and Therapeutic Opportunities.Molecular and cellular biology · 2025Review
- Post-transcriptional checkpoints in autoimmunity.Nature reviews. Rheumatology · 2023Review
- HuR as a molecular target for cancer therapeutics and immune-related disorders.Advanced drug delivery reviews · 2022Review
- The effects of modified RNA-binding proteins HuR on the biological behavior of the bladder cancer T24 cell line.Translational andrology and urology · 2022Article
- Drug delivery approaches for HuR-targeted therapy for lung cancer.Advanced drug delivery reviews · 2022Review
- The RNA-binding protein HuR is required for maintenance of the germinal centre response.Nature communications · 2021Article
- Generation and characterization of CD19-iCre mice as a tool for efficient and specific conditional gene targeting in B cells.Scientific reports · 2021Article
- RNA-Binding Protein HuR Promotes Th17 Cell Differentiation and Can Be Targeted to Reduce Autoimmune Neuroinflammation.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Adipose HuR protects against diet-induced obesity and insulin resistance.Nature communications · 2019Article
- HuR controls apoptosis and activation response without effects on cytokine 3' UTRs.RNA biology · 2019Article
- Alternative-splicing defects in cancer: Splicing regulators and their downstream targets, guiding the way to novel cancer therapeutics.Wiley interdisciplinary reviews. RNA · 2018Review
- RNA-binding proteins control gene expression and cell fate in the immune system.Nature immunology · 2018Review
- Uncovering the Role of RNA-Binding Proteins in Gene Expression in the Immune System.Frontiers in immunology · 2018Review
- Regulation of HuR structure and function by dihydrotanshinone-I.Nucleic acids research · 2017Article
- Cell cycle RNA regulons coordinating early lymphocyte development.Wiley interdisciplinary reviews. RNA · 2017Review
- Alternative splicing: the pledge, the turn, and the prestige : The key role of alternative splicing in human biological systems.Human genetics · 2017Review
- Hallmarks of cancer and AU-rich elements.Wiley interdisciplinary reviews. RNA · 2017Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
The HuR RNA-binding protein posttranscriptionally controls expression of genes involved in cellular survival, proliferation, and differentiation. To determine roles of HuR in B cell development and function, we analyzed mice with B lineage-specific deletion of the HuR gene. These HuRΔ/Δ mice have reduced numbers of immature bone marrow and mature splenic B cells, with only the former rescued by p53 inactivation, indicating that HuR supports B lineage cells through developmental stage-specific mechanisms. Upon in vitro activation, HuRΔ/Δ B cells have a mild proliferation defect and impaired ability to produce mRNAs that encode IgH chains of secreted Abs, but no deficiencies in survival, isotype switching, or expression of germinal center (GC) markers. In contrast, HuRΔ/Δ mice have minimal serum titers of all Ab isotypes, decreased numbers of GC and plasma B cells, and few peritoneal B-1 B cells. Moreover, HuRΔ/Δ mice have severely decreased GCs, T follicular helper cells, and high-affinity Abs after immunization with a T cell-dependent Ag. This failure of HuRΔ/Δ mice to mount a T cell-dependent Ab response contrasts with the ability of HuRΔ/Δ B cells to become GC-like in vitro, indicating that HuR is essential for aspects of B cell activation unique to the in vivo environment. Consistent with this notion, we find in vitro stimulated HuRΔ/Δ B cells exhibit modestly reduced surface expression of costimulatory molecules whose expression is similarly decreased in humans with common variable immunodeficiency. HuRΔ/Δ mice provide a model to identify B cell-intrinsic factors that promote T cell-dependent immune responses in vivo.
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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.