ArticleAmerican journal of physiology. Cell physiology2015
TRA2β controls Mypt1 exon 24 splicing in the developmental maturation of mouse mesenteric artery smooth muscle.
Article in American journal of physiology. Cell physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 18 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
- Bioinformatic analysis of smoothelin family members supports tissue-specific functions of unique C-terminal calponin homology domains.Physiological reports · 2023Article
- Transformer 2β regulates the alternative splicing of cell cycle regulatory genes to promote the malignant phenotype of ovarian cancer.Oncology research · 2023Article
- Clinical and Molecular Insights into Gastrointestinal Dysfunction in Myotonic Dystrophy Types 1 & 2.International journal of molecular sciences · 2022Review
- 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
- Editing of the myosin phosphatase regulatory subunit suppresses angiotensin II induced hypertension via sensitization to nitric oxide mediated vasodilation.Pflugers Archiv : European journal of physiology · 2021Article
- Muscle developmental defects in heterogeneous nuclear Ribonucleoprotein A1 knockout mice.Open biology · 2017Article
- 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
- Unique gene program of rat small resistance mesenteric arteries as revealed by deep RNA sequencing.Physiological reports · 2015Article
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 at 2 institutions in 2 countries.
Funding
Abstract
Diversity of smooth muscle within the vascular system is generated by alternative splicing of exons, yet there is limited understanding of its timing or control mechanisms. We examined splicing of myosin phosphatase regulatory subunit (Mypt1) exon 24 (E24) in relation to smooth muscle myosin heavy chain (Smmhc) and smoothelin (Smtn) alternative exons (Smmhc E6 and Smtn E20) during maturation of mouse mesenteric artery (MA) smooth muscle. The role of transformer 2β (Tra2β), a master regulator of splicing in flies, in maturation of arterial smooth muscle was tested through gene inactivation. Splicing of alternative exons in bladder smooth muscle was examined for comparative purposes. MA smooth muscle maturation began after postnatal week 2 and was complete at maturity, as indicated by switching to Mypt1 E24+ and Smtn E20- splice variants and 11-fold induction of Smmhc. Similar changes in bladder were complete by postnatal day 3. Splicing of Smmhc E6 was temporally dissociated from Mypt1 E24 and Smtn E20 and discordant between arteries and bladder. Tamoxifen-induced smooth muscle-specific inactivation of Tra2β within the first week of life but not in maturity reduced splicing of Mypt1 E24 in MAs. Inactivation of Tra2β causing a switch to the isoform of MYPT1 containing the COOH-terminal leucine zipper motif (E24-) increased arterial sensitivity to cGMP-mediated relaxation. In conclusion, maturation of mouse MA smooth muscle begins postnatally and continues until sexual maturity. TRA2β is required for specification during this period of maturation, and its inactivation alters the contractile properties of mature arterial smooth muscle.
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.