ArticleThe Journal of biological chemistry2012
Tra2β protein is required for tissue-specific splicing of a smooth muscle myosin phosphatase targeting subunit alternative exon.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 22 citations in OpenAlex.
- MBNL loss of function in smooth muscle as a model for myotonic dystrophy associated gastrointestinal dysmotility.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- 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
- Review
- The alternative splicing program of differentiated smooth muscle cells involves concerted non-productive splicing of post-transcriptional regulators.Nucleic acids research · 2016Article
- 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
- Limited miR-17-92 overexpression drives hematologic malignancies.Leukemia research · 2015Article
- TRA2β controls Mypt1 exon 24 splicing in the developmental maturation of mouse mesenteric artery smooth muscle.American journal of physiology. Cell physiology · 2015Article
- In vivo roles for myosin phosphatase targeting subunit-1 phosphorylation sites T694 and T852 in bladder smooth muscle contraction.The Journal of physiology · 2015Article
- Transformer 2β homolog (Drosophila) (TRA2B) regulates protein kinase C δI (PKCδI) splice variant expression during 3T3L1 preadipocyte cell cycle.The Journal of biological chemistry · 2014Article
- Neural programming of mesenteric and renal arteries.American journal of physiology. Heart and circulatory physiology · 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
- The expression analysis of Sfrs10 and Celf4 during mouse retinal development.Gene expression patterns : GEP · 2013Article
- Impaired contractile responses and altered expression and phosphorylation of Ca(2+) sensitization proteins in gastric antrum smooth muscles from ob/ob mice.Journal of muscle research and cell motility · 2013Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Alternative splicing of the smooth muscle myosin phosphatase targeting subunit (Mypt1) exon 23 (E23) is tissue-specific and developmentally regulated and, thus, an attractive model for the study of smooth muscle phenotypic specification. We have proposed that Tra2β functions as a tissue-specific activator of Mypt1 E23 splicing on the basis of concordant expression patterns and Tra2β activation of Mypt1 E23 mini-gene splicing in vitro. In this study we examined the relationship between Tra2β and Mypt1 E23 splicing in vivo in the mouse. Tra2β was 2- to 5-fold more abundant in phasic smooth muscle tissues, such as the portal vein, small intestine, and small mesenteric artery, in which Mypt1 E23 is predominately included as compared with the tonic smooth muscle tissues, such as the aorta and inferior vena cava, in which Mypt1 E23 is predominately skipped. Tra2β was up-regulated in the small intestine postnatally, concordant with a switch to Mypt1 E23 splicing. Targeting of Tra2β in smooth muscle cells using SM22α-Cre caused a substantial reduction in Mypt1 E23 inclusion specifically in the intestinal smooth muscle of heterozygotes, indicating sensitivity to Tra2β gene dosage. The switch to the Mypt1 E23 skipped isoform coding for the C-terminal leucine zipper motif caused increased sensitivity of the muscle to the relaxant effects of 8-Br-cyclic guanosine monophosphate (cGMP). We conclude that Tra2β is necessary for the tissue-specific splicing of Mypt1 E23 in the phasic intestinal smooth muscle. Tra2β, by regulating the splicing of Mypt1 E23, sets the sensitivity of smooth muscle to cGMP-mediated relaxation.
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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.