ArticleJournal of cellular biochemistry2012
Comprehensive analysis of titin protein isoform and alternative splicing in normal and mutant rats.
Article in Journal of cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- MyoMed205 Counteracts Titin Hyperphosphorylation and the Expression of Contraction-Regulating Proteins in a Rat Model of HFpEF.Journal of cachexia, sarcopenia and muscle · 2025Article
- Titin is a new factor regulating arterial stiffness through vascular smooth muscle cell tone in male rats.Physiological reports · 2025Article
- Visualizing sarcomere and cellular dynamics in skeletal muscle to improve cell therapies.eLife · 2024Article
- Expression of Smyd1b_tv1 by Alternative Splicing in Cardiac Muscle is Critical for Sarcomere Organization in Cardiomyocytes and Heart Function.Molecular and cellular biology · 2024Article
- Thick filament activation is different in fast- and slow-twitch skeletal muscle.The Journal of physiology · 2022Article
- Bridging the muscle genome to phenome across multiple biological scales.The Journal of experimental biology · 2022Article
- The titin N2B and N2A regions: biomechanical and metabolic signaling hubs in cross-striated muscles.Biophysical reviews · 2021Review
- The ryanodine receptor stabilizer S107 ameliorates contractility of adult Rbm20 knockout rat cardiomyocytes.Physiological reports · 2021Article
- RBM20-Mediated Pre-mRNA Splicing Has Muscle-Specificity and Differential Hormonal Responses between Muscles and in Muscle Cell Cultures.International journal of molecular sciences · 2021Article
- Effects of S-glutathionylation on the passive force-length relationship in skeletal muscle fibres of rats and humans.Journal of muscle research and cell motility · 2020Article
- Review
- Megaesophagus Is a Major Pathological Condition in Rats With a Large Deletion in theVeterinary pathology · 2020Article
- Compliant Titin Isoform Content Is Reduced in Left Ventricles of Sedentary Versus Active Rats.Frontiers in physiology · 2020Article
- Deleting Titin's C-Terminal PEVK Exons Increases Passive Stiffness, Alters Splicing, and Induces Cross-Sectional and Longitudinal Hypertrophy in Skeletal Muscle.Frontiers in physiology · 2020Article
- Training Induced Changes to Skeletal Muscle Passive Properties Are Evident in Both Single Fibers and Fiber Bundles in the Rat Hindlimb.Frontiers in physiology · 2020Article
- Resolving titin's lifecycle and the spatial organization of protein turnover in mouse cardiomyocytes.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Z-band and M-band titin splicing and regulation by RNA binding motif 20 in striated muscles.Journal of cellular biochemistry · 2018Article
- RBM20, a potential target for treatment of cardiomyopathy via titin isoform switching.Biophysical reviews · 2018Review
- Review
- Nuances of electrophoresis study of titin/connectin.Biophysical reviews · 2017Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Titin is a giant protein with multiple functions in cardiac and skeletal muscles. Rat cardiac titin undergoes developmental isoform transition from the neonatal 3.7 MDa N2BA isoform to primarily the adult 2.97 MDa N2B isoform. An autosomal dominant mutation dramatically altered this transformation. Titins from eight skeletal muscles: Tibialis Anterior (TA), Longissimus Dorsi (LD) and Gastrocnemius (GA), Extensor Digitorum Longus (ED), Soleus (SO), Psoas (PS), Extensor Oblique (EO), and Diaphram (DI) were characterized in wild type and in homozygous mutant (Hm) rats with a titin splicing defect. Results showed that the developmental reduction in titin size is eliminated in the mutant rat so that the titins in all investigated skeletal muscles remain large in the adult. The alternative splicing of titin mRNA was found repressed by this mutation, a result consistent with the large titin isoform in the mutant. The developmental pattern of titin mRNA alternative splicing differs between heart and skeletal muscles. The retention of intron 49 reveals a possible mechanism for the absence of the N2B unique region in the expressed titin protein of skeletal muscle.
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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.