ArticleNature2013
ZFP36L2 is required for self-renewal of early burst-forming unit erythroid progenitors.
Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.
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Who cites it
85 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.
- Comprehensive Gene expression meta-analysis and integrated bioinformatic approaches reveal shared signatures between thrombosis and myeloproliferative disorders.Scientific reports · 2016Pooled it
- Article
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- ZFP36 Family Proteins as Critical Regulators of Inflammation, Immune Cell Development, and Antiviral Responses.Vaccines · 2026Review
- ZFP36L1 and ZFP36L2 cooperatively regulate thymic epithelial cell function to prevent early-onset thymic involution.Cell death and differentiation · 2026Article
- Molecular and therapeutic frontiers in anemia therapy.The Journal of clinical investigation · 2026Review
- Deficiency of ZFP36L1 and ZFP36L2 impairs liver homeostasis and initiates cholestatic liver injury.Hepatology communications · 2026Article
- Regulation of Alternative Polyadenylation Events by PABPC1 Affects Erythroid Progenitor Cell Expansion.Genomics, proteomics & bioinformatics · 2025Article
- Identification of deleterious non-synonymous single nucleotide polymorphisms in the mRNA decay activator ZFP36L2.RNA biology · 2025Article
- The interplay between driver mutation and oxidative stress in colorectal cancer: from pathogenesis to therapeutics.Journal of translational medicine · 2025Review
- Article
- The glucocorticoid receptor elicited proliferative response in human erythropoiesis is BCL11A-dependent.Stem cells (Dayton, Ohio) · 2024Article
- Targeting the glucocorticoid receptor-CCR8 axis mediated bone marrow T cell sequestration enhances infiltration of anti-tumor T cells in intracranial cancers.Cellular & molecular immunology · 2024Article
- Fasting reshapes tissue-specific niches to improve NK cell-mediated anti-tumor immunity.Immunity · 2024Article
- Abundant binary promoter switches in lineage-determining transcription factors indicate a digital component of cell fate determination.Cell reports · 2023Article
- AhR and CYP1B1 Control Oxygen Effects on Bone Marrow Progenitor Cells: The Enrichment of Multiple Olfactory Receptors as Potential Microbiome Sensors.International journal of molecular sciences · 2023Article
- Associations of obesity and body shape with erythrocyte and reticulocyte parameters in the UK Biobank cohort.BMC endocrine disorders · 2023Article
- Type 2 inflammation drives an airway basal stem cell program through insulin receptor substrate signaling.The Journal of allergy and clinical immunology · 2023Article
- Patients with hypercortisolemic Cushing disease possess a distinct class of hematopoietic progenitor cells leading to erythrocytosis.Haematologica · 2023Article
- The RNA binding proteinsFrontiers in cell and developmental biology · 2023Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Stem cells and progenitors in many lineages undergo self-renewing divisions, but the extracellular and intracellular proteins that regulate this process are largely unknown. Glucocorticoids stimulate red blood cell formation by promoting self-renewal of early burst-forming unit-erythroid (BFU-E) progenitors. Here we show that the RNA-binding protein ZFP36L2 is a transcriptional target of the glucocorticoid receptor (GR) in BFU-Es and is required for BFU-E self-renewal. ZFP36L2 is normally downregulated during erythroid differentiation from the BFU-E stage, but its expression is maintained by all tested GR agonists that stimulate BFU-E self-renewal, and the GR binds to several potential enhancer regions of ZFP36L2. Knockdown of ZFP36L2 in cultured BFU-E cells did not affect the rate of cell division but disrupted glucocorticoid-induced BFU-E self-renewal, and knockdown of ZFP36L2 in transplanted erythroid progenitors prevented expansion of erythroid lineage progenitors normally seen following induction of anaemia by phenylhydrazine treatment. ZFP36L2 preferentially binds to messenger RNAs that are induced or maintained at high expression levels during terminal erythroid differentiation and negatively regulates their expression levels. ZFP36L2 therefore functions as part of a molecular switch promoting BFU-E self-renewal and a subsequent increase in the total numbers of colony-forming unit-erythroid (CFU-E) progenitors and erythroid cells that are generated.
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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.