ArticlePloS one2015
Deletion of AU-rich elements within the Bcl2 3'UTR reduces protein expression and B cell survival in vivo.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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
7 citing papers in PubMed, 16 citations in OpenAlex.
- 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
- Plant 3' Regulatory Regions From mRNA-Encoding Genes and Their Uses to Modulate Expression.Frontiers in plant science · 2020Review
- hnRNP L-dependent protection of normal mRNAs from NMD subverts quality control in B cell lymphoma.The EMBO journal · 2019Article
- Negative Regulation of BOK Expression by Recruitment of TRIM28 to Regulatory Elements in Its 3' Untranslated Region.iScience · 2018Article
- Uncovering the Role of RNA-Binding Proteins in Gene Expression in the Immune System.Frontiers in immunology · 2018Review
- Tia1 dependent regulation of mRNA subcellular location and translation controls p53 expression in B cells.Nature communications · 2017Article
- RNA binding proteins as regulators of immune cell biology.Clinical and experimental immunology · 2016Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Post-transcriptional mRNA regulation by RNA binding proteins (RBPs) associated with AU-rich elements (AREs) present in the 3' untranslated region (3'UTR) of specific mRNAs modulates transcript stability and translation in eukaryotic cells. Here we have functionally characterised the importance of the AREs present within the Bcl2 3'UTR in order to maintain Bcl2 expression. Gene targeting deletion of 300 nucleotides of the Bcl2 3'UTR rich in AREs diminishes Bcl2 mRNA stability and protein levels in primary B cells, decreasing cell lifespan. Generation of chimeric mice indicates that Bcl2-ARE∆/∆ B cells have an intrinsic competitive disadvantage compared to wild type cells. Biochemical assays and predictions using a bioinformatics approach show that several RBPs bind to the Bcl2 AREs, including AUF1 and HuR proteins. Altogether, association of RBPs to Bcl2 AREs contributes to Bcl2 protein expression by stabilizing Bcl2 mRNA and promotes B cell maintenance.
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Registered trials
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