ReviewCurrent opinion in hematology2017
RNA splicing during terminal erythropoiesis.
Review in Current opinion in hematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Immune-associated alternative splicing signatures define molecular subtypes in breast cancer.iScience · 2026Article
- A NovelAnnals of laboratory medicine · 2026Article
- Multi-omics approaches reveal erythroid progenitor cell in cancer: from passive bystander to active player.Oncogene · 2026Review
- Prpf4 sequentially regulates the expansion and maturation of erythrocyte through distinct mechanisms.Cell death discovery · 2025Article
- TET dioxygenases localize at splicing speckles and promote RNA splicing.Nucleus (Austin, Tex.) · 2025Article
- Exploring the connection between RNA splicing and intellectual disability.Current opinion in genetics & development · 2025Review
- Splicing the Difference: Harnessing the Complexity of the Transcriptome in Hematopoiesis.Experimental hematology · 2024Review
- Small-molecule α-lipoic acid targets ELK1 to balance human neutrophil and erythrocyte differentiation.Stem cell research & therapy · 2024Article
- The transcriptomic landscape of normal and ineffective erythropoiesis at single-cell resolution.Blood advances · 2023Article
- Post-transcriptional regulation of erythropoiesis.Blood science (Baltimore, Md.) · 2023Review
- Dynamic changes in RNA-protein interactions and RNA secondary structure in mammalian erythropoiesis.Life science alliance · 2021Article
- Article
- Aberrant splicing contributes to severe α-spectrin-linked congenital hemolytic anemia.The Journal of clinical investigation · 2019Article
- Blood Relatives: Splicing Mechanisms underlying Erythropoiesis in Health and Disease.F1000Research · 2018Review
- Alternative splicing as a regulator of development and tissue identity.Nature reviews. Molecular cell biology · 2017Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
purpose of reviewErythroid progenitors must accurately and efficiently splice thousands of pre-mRNAs as the cells undergo extensive changes in gene expression and cellular remodeling during terminal erythropoiesis. Alternative splicing choices are governed by interactions between RNA binding proteins and cis-regulatory binding motifs in the RNA. This review will focus on recent studies that define the genome-wide scope of splicing in erythroblasts and discuss what is known about its regulation. RECENT
findingsRNA-seq analysis of highly purified erythroblast populations has revealed an extensive program of alternative splicing of both exons and introns. During normal erythropoiesis, stage-specific splicing transitions alter the structure and abundance of protein isoforms required for optimized red cell production. Mutation or deficiency of splicing regulators underlies hematopoietic disease in myelopdysplasia syndrome patients via disrupting the splicing program. SUMMARY: Erythroid progenitors execute an elaborate alternative splicing program that modulates gene expression posttranscriptionally, ultimately regulating the structure and function of the proteome in a differentiation stage-specific manner during terminal erythropoiesis. This program helps drive differentiation and ensure synthesis of the proper protein isoforms required to produce mechanically stable red cells. Mutation or deficiency of key splicing regulatory proteins disrupts the splicing program to cause disease.
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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.