ArticleMolecular and cellular biology2006
BRF1 protein turnover and mRNA decay activity are regulated by protein kinase B at the same phosphorylation sites.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 89 citations in OpenAlex.
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- Differential Regulation of TCR-Induced ZFP36 and ZFP36L1 Expression by Cyclosporin A in CD8European journal of immunology · 2025Article
- 1-L Transcription in Prion Diseases.International journal of molecular sciences · 2024Article
- Regulation of low-density lipoprotein receptor expression in triple negative breast cancer by EGFR-MAPK signaling.Scientific reports · 2021Article
- The Emerging Role of Stress Granules in Hepatocellular Carcinoma.International journal of molecular sciences · 2021Review
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- mRNA Post-Transcriptional Regulation by AU-Rich Element-Binding Proteins in Liver Inflammation and Cancer.International journal of molecular sciences · 2020Review
- RNA-Binding Proteins in Acute Leukemias.International journal of molecular sciences · 2020Review
- AU-rich element-mediated mRNA decay via the butyrate response factor 1 controls cellular levels of polyadenylated replication-dependent histone mRNAs.The Journal of biological chemistry · 2019Article
- IL-33 regulates cytokine production and neutrophil recruitment via the p38 MAPK-activated kinases MK2/3.Immunology and cell biology · 2019Article
- Alcohol Intake and Abnormal Expression of Brf1 in Breast Cancer.Oxidative medicine and cellular longevity · 2019Review
- Emerging Evidence of Translational Control by AU-Rich Element-Binding Proteins.Frontiers in genetics · 2019Review
- Cell cycle RNA regulons coordinating early lymphocyte development.Wiley interdisciplinary reviews. RNA · 2017Review
- The cAMP pathway regulates mRNA decay through phosphorylation of the RNA-binding protein TIS11b/BRF1.Molecular biology of the cell · 2016Article
- The control of inflammation via the phosphorylation and dephosphorylation of tristetraprolin: a tale of two phosphatases.Biochemical Society transactions · 2016Review
- RNA binding proteins as regulators of immune cell biology.Clinical and experimental immunology · 2016Review
- Post-transcriptional Regulation of Immunological Responses through Riboclustering.Frontiers in immunology · 2016Review
- mTOR regulates MAPKAPK2 translation to control the senescence-associated secretory phenotype.Nature cell biology · 2015Article
- Novel roles for LIX1L in promoting cancer cell proliferation through ROS1-mediated LIX1L phosphorylation.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BRF1 posttranscriptionally regulates mRNA levels by targeting ARE-bearing transcripts to the decay machinery. We previously showed that protein kinase B (PKB) phosphorylates BRF1 at Ser92, resulting in binding to 14-3-3 and impairment of mRNA decay activity. Here we identify an additional regulatory site at Ser203 that cooperates in vivo with Ser92. In vitro kinase labeling and wortmannin sensitivity indicate that Ser203 phosphorylation is also performed by PKB. Mutation of both serines to alanine uncouples BRF1 from PKB regulation, leading to constitutive mRNA decay even in the presence of stabilizing signals. BRF1 protein is labile because of proteasomal degradation (half-life, <3 h) but becomes stabilized upon phosphorylation and is less stable in PKBalpha(-/-) cells. Surprisingly, phosphorylation-dependent protein stability is also regulated by Ser92 and Ser203, with parallel phosphorylation required at these sites. Phosphorylation-dependent binding to 14-3-3 is abolished only when both sites are mutated. Cell compartment fractionation experiments support a model in which binding to 14-3-3 sequesters BRF1 through relocalization and prevents it from executing its mRNA decay activity, as well as from proteasomal degradation, thereby maintaining high BRF1 protein levels that are required to reinstate decay upon dissipation of the stabilizing signal.
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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.