ArticleCirculation research2008
Tra2beta as a novel mediator of vascular smooth muscle diversification.
Article in Circulation research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 34 citations in OpenAlex.
- Dual Role of Transformer 2 Beta as Both a Developmental Necessity and a Disease Modulator.International journal of molecular sciences · 2025Review
- An antisense oligonucleotide efficiently suppresses splicing of an alternative exon in vascular smooth muscle in vivo.American journal of physiology. Heart and circulatory physiology · 2024Article
- Aging related decreases in NM myosin expression and contractility in a resistance vessel.Frontiers in physiology · 2024Article
- Review
- Myocardin regulates exon usage in smooth muscle cells through induction of splicing regulatory factors.Cellular and molecular life sciences : CMLS · 2022Article
- Tissue-specific expression of myosin phosphatase subunits and isoforms in smooth muscle of mice and humans.American journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
- HnRNPA1 interacts with G-quadruplex in the TRA2B promoter and stimulates its transcription in human colon cancer cells.Scientific reports · 2019Article
- Article
- The alternative splicing program of differentiated smooth muscle cells involves concerted non-productive splicing of post-transcriptional regulators.Nucleic acids research · 2016Article
- A splice variant of the myosin phosphatase regulatory subunit tunes arterial reactivity and suppresses response to salt loading.American journal of physiology. Heart and circulatory physiology · 2016Article
- Mechanisms of Vascular Smooth Muscle Contraction and the Basis for Pharmacologic Treatment of Smooth Muscle Disorders.Pharmacological reviews · 2016Review
- Redox signaling and splicing dependent change in myosin phosphatase underlie early versus late changes in NO vasodilator reserve in a mouse LPS model of sepsis.American journal of physiology. Heart and circulatory physiology · 2015Article
- TRA2β controls Mypt1 exon 24 splicing in the developmental maturation of mouse mesenteric artery smooth muscle.American journal of physiology. Cell physiology · 2015Article
- Transformer 2β (Tra2β/SFRS10) positively regulates the progression of NSCLC via promoting cell proliferation.Journal of molecular histology · 2014Article
- A bioinformatic and computational study of myosin phosphatase subunit diversity.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- Myosin phosphatase isoforms as determinants of smooth muscle contractile function and calcium sensitivity of force production.Microcirculation (New York, N.Y. : 1994) · 2014Review
- Neuronal-specific deficiency of the splicing factor Tra2b causes apoptosis in neurogenic areas of the developing mouse brain.PloS one · 2014Article
- The expression analysis of Sfrs10 and Celf4 during mouse retinal development.Gene expression patterns : GEP · 2013Article
- Characterization of nuclear localization signals (NLSs) and function of NLSs and phosphorylation of serine residues in subcellular and subnuclear localization of transformer-2β (Tra2β).The Journal of biological chemistry · 2013Article
- Tra2β protein is required for tissue-specific splicing of a smooth muscle myosin phosphatase targeting subunit alternative exon.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Transformer splicing regulatory proteins determine the sexually dimorphic traits of Drosophila. The role of the vertebrate homologs of Tra-2 in phenotypic specification is undefined. We are using the alternative splicing of the MYPT1 E23 exon as a model for the study of smooth muscle diversification into fast and slow contractile phenotypes. Tra2beta mRNA and protein is expressed at up to 10-fold higher levels in fast smooth muscle tissues such as the rat portal vein and small mesenteric artery, in which E23 is spliced, as compared to the slow smooth muscle tissues of the large arteries and veins, in which E23 is skipped. Tra2beta is upregulated up to 10-fold concordant with the initiation of E23 splicing as the rat portal vein and avian gizzard implement the fast program of gene expression in the perinatal period. In disease models such as portal hypertension and mesenteric artery high/low flow, the portal vein and first order mesenteric artery dynamically downregulate Tra2beta concordant with a shift to E23 skipping and the slow program of gene expression. Tra2beta binds to a highly conserved sequence within E23 and transactivates its splicing in vitro and in vivo; this is abolished with mutation or deletion of this sequence. RNA interference-mediated knockdown of Tra2beta markedly reduces E23 splicing. We propose that Tra2beta has been conserved through evolution and redeployed for the specification of the fast smooth muscle phenotype and may serve as a novel nodal point for the investigation of this process in developmental and disease models.
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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.