ArticleExperimental hematology2014
Deletion of Dicer in late erythroid cells results in impaired stress erythropoiesis in mice.
Article in Experimental hematology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Exploring unconventional attributes of red blood cells and their potential applications in biomedicine.Protein & cell · 2024Article
- Hematologic indices in individuals with pathogenic germline DICER1 variants.Blood advances · 2021Review
- Article
- Creating conditional dual fluorescence labeled transgenic animals for studying function of small noncoding RNAs.Connective tissue research · 2017Article
- Adenosine-to-inosine RNA editing by ADAR1 is essential for normal murine erythropoiesis.Experimental hematology · 2016Article
- A comprehensive joint analysis of the long and short RNA transcriptomes of human erythrocytes.BMC genomics · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
MicroRNAs (miRNAs) have been shown to influence erythroid lineage commitment and differentiation; however, our knowledge of miRNA function in terminal erythropoiesis remains limited. To address this issue, we generated a novel animal model, where the miRNA-processing enzyme, Dicer, is selectively inactivated in erythropoietin receptor positive erythroid cells beginning with CFU-e/proerythroblast cells. This results in significant depletion of all miRNAs from the proerythroblast stage onwards, with one exception, miR-451, which is processed by Ago2 in a Dicer-independent manner. We observed that mature Dicer-dependent miRNAs, like miR-451, are dispensable under steady-state conditions, but these mutants have an impaired response to stress erythropoiesis, as demonstrated by a delay in recovery from anemia. This defect was specific to later maturing erythroid cells, as progenitor numbers were unaffected. In addition to generating a novel mouse model to study miRNA function in late erythroid cells, we conclude that miRNAs (both Dicer-dependent and independent) act primarily to regulate the optimal response to stress among late erythroid cells.
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Registered trials
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