ArticleBlood2008
Regulated Fox-2 isoform expression mediates protein 4.1R splicing during erythroid differentiation.
Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
29 citing papers in PubMed.
- RBFOX2-dependent alternative splicing of Numb regulates Notch signaling during muscle stem cell activation.Stem cell reports · 2026Article
- RNA splicing factor RBFOX2 is a key factor in the progression of cancer and cardiomyopathy.Clinical and translational medicine · 2024Review
- RBFOX2 as a regulatory linchpin in cancer: insights from a comprehensive review of its roles in tumorigenesis.American journal of cancer research · 2024Review
- Splicing regulation of GFPT1 muscle-specific isoform and its roles in glucose metabolisms and neuromuscular junction.iScience · 2023Article
- Article
- RNA splicing during terminal erythropoiesis.Current opinion in hematology · 2017Review
- Protein 4.1R Exon 16 3' Splice Site Activation Requires Coordination among TIA1, Pcbp1, and RBM39 during Terminal Erythropoiesis.Molecular and cellular biology · 2017Article
- Satellite-like cells contribute to pax7-dependent skeletal muscle repair in adult zebrafish.Developmental biology · 2017Article
- HnRNP A1 tethers KSRP to an exon splicing silencer that inhibits an erythroid-specific splicing event in PU.1-induced erythroleukemia.American journal of cancer research · 2015Article
- Article
- A dynamic alternative splicing program regulates gene expression during terminal erythropoiesis.Nucleic acids research · 2014Article
- Article
- The RNA binding protein RBM38 (RNPC1) regulates splicing during late erythroid differentiation.PloS one · 2013Article
- Article
- The splicing regulator Rbfox2 is required for both cerebellar development and mature motor function.Genes & development · 2012Article
- RBFOX2 promotes protein 4.1R exon 16 selection via U1 snRNP recruitment.Molecular and cellular biology · 2012Article
- Abnormal mitoferrin-1 expression in patients with erythropoietic protoporphyria.Experimental hematology · 2011Article
- Fox-3 and PSF interact to activate neural cell-specific alternative splicing.Nucleic acids research · 2011Article
- Efficient in vivo manipulation of alternative pre-mRNA splicing events using antisense morpholinos in mice.The Journal of biological chemistry · 2011Article
- Comprehensive analysis of alternative splicing and functionality in neuronal differentiation of P19 cells.PloS one · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
A regulated splicing event in protein 4.1R pre-mRNA-the inclusion of exon 16-encoding peptides for spectrin-actin binding-occurs in late erythroid differentiation. We defined the functional significance of an intronic splicing enhancer, UGCAUG, and its cognate splicing factor, mFox2A, on exon 16 splicing during differentiation. UGCAUG displays cell-type-specific splicing regulation in a test neutral reporter and has a dose-dependent enhancing effect. Erythroid cells express 2 UGCAUG-binding mFox-2 isoforms, an erythroid differentiation-inducible mFox-2A and a commonly expressed mFox-2F. When overexpressed, both enhanced internal exon splicing in an UGCAUG-dependent manner, with mFox-2A exerting a much stronger effect than mFox-2F. A significant reciprocal increase in mFox-2A and decrease in mFox-2F occurred during erythroid differentiation and correlated with exon 16 inclusion. Furthermore, isoform-specific expression reduction reversed mFox-2A-enhancing activity, but not that of mFox-2F on exon 16 inclusion. Our results suggest that an erythroid differentiation-inducible mFox-2A isoform is a critical regulator of the differentiation-specific exon 16 splicing switch, and that its up-regulation in late erythroid differentiation is vital for exon 16 splicing.
Indexed as
Identifiers
What OpenQuestion holds
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.