Troponin T (TnT) is a key protein for Ca(2+)-sensitive molecular switching of muscle contraction. In vertebrates, three TnT genes have been identified, which produce isoforms characteristic of cardiac, fast skeletal, and slow skeletal muscles through alternative splicing in a tissue-specific and developmentally regulated manner. The diversification of myofibers into forms with specific metabolic and contractile characteristics is thought to be closely associated with the differential expression of these TnT isoforms. Herein, we determined the nucleotide sequence of the chicken slow skeletal muscle TnT gene and its upstream region. The gene was simpler in structure than the two other chicken genes. The transcription initiation site was positioned 183 bp upstream of the 3' end of exon 1. Alternative splicing of exon 5 using an internal acceptor site generated two distinct slow skeletal muscle troponin T (sTnT) transcripts. We identified possible regulatory elements, M-CAT-like, CACC-box, and E-box (E-box1 to E-box3) motifs in the upstream region and an E-box motif (E-box4) in exon 1.
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http://dx.doi.org/10.1016/j.gene.2004.05.023 | DOI Listing |
Biomolecules
December 2024
Department of Aerospace Medical Training, School of Aerospace Medicine, Fourth Military Medical University, Xi'an 710032, China.
Skeletal muscle atrophy, which is induced by factors such as disuse, spaceflight, certain medications, neurological disorders, and malnutrition, is a global health issue that lacks effective treatment. Hindlimb unloading is a commonly used model of muscle atrophy. However, the underlying mechanism of muscle atrophy induced by hindlimb unloading remains unclear, particularly from the perspective of the myocyte proteome and metabolism.
View Article and Find Full Text PDFJ Anat
January 2025
Institute of Sports Medicine Copenhagen, Department of Orthopedic Surgery, Copenhagen University Hospital - Bispebjerg-Frederiksberg, Copenhagen, Denmark.
Tendon injuries and disorders associated with mechanical tendon overuse are common musculoskeletal problems. Even though tendons play a central role in human movement, the intrinsic healing process of tendon is very slow. So far, it is known that tendon cell activity is supported by several interstitial cells within the tendon.
View Article and Find Full Text PDFPathophysiology
January 2025
Postgraduate Program in Health Sciences, Faculty of Medicine of Jundiaí (FMJ), Jundiaí 13202-550, Brazil.
Duchenne muscular dystrophy (DMD) is a genetic disease characterized by a lack of dystrophin caused by mutations in the DMD gene, and some minor cases are due to decreased levels of dystrophin, leading to muscle weakness and motor impairment. Creatine supplementation has demonstrated several benefits for the muscle, such as increased strength, enhanced tissue repair, and improved ATP resynthesis. This preliminary study aimed to investigate the effects of creatine on the gastrocnemius muscle in dystrophy muscle (MDX) and healthy C57BL/10 mice.
View Article and Find Full Text PDFIran J Med Sci
December 2024
Department of Oral and Maxillofacial Radiology, School of Dentistry, Tehran University of Medical Sciences, Tehran, Iran.
Fibrous dysplasia is a slow-progressing benign condition characterized by abnormal bone formation that leads to some skeletal disorders. Although some of the fibrous dysplasia have unusual clinical and radiographic features that can lead to a challenging diagnosis, most lesions reveal an expansile bone defect due to cortex thinning. This report presented a case of monostotic fibrous dysplasia of a 43-year-old woman with involvement of the right maxillary jaw and sinuses, which indicated unusual histopathological features.
View Article and Find Full Text PDFJ Clin Invest
January 2025
Center for Inherited Myology Research, Virginia Commonwealth University, Richmond, United States of America.
Background: Myotonic dystrophy type 1 (DM1) is a multisystemic, CTG repeat expansion disorder characterized by a slow, progressive decline in skeletal muscle function. A biomarker correlating RNA mis-splicing, the core pathogenic disease mechanism, and muscle performance is crucial for assessing response to disease-modifying interventions. We evaluated the Myotonic Dystrophy Splice Index (SI), a composite RNA splicing biomarker incorporating 22 disease-specific events, as a potential biomarker of DM1 muscle weakness.
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