Human myosin heavy chains are encoded by a multigene family consisting of at least 10 members. A gene-specific oligonucleotide has been used to isolate the human beta myosin heavy chain gene from a group of twelve nonoverlapping genomic clones. We have shown that this gene (which is expressed in both cardiac and skeletal muscle) is located 3.6kb upstream of the alpha cardiac myosin gene. We find that DNA sequences located upstream of rat and human alpha cardiac myosin heavy chain genes are very homologous over a 300bp region. Analogous regions of two other myosin genes expressed in different muscles (cardiac and skeletal) show no such homology to each other. While a human skeletal muscle myosin heavy chain gene cluster is located on chromosome 17, we show that the beta and alpha human cardiac myosin heavy chain genes are located on chromosome 14.
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http://dx.doi.org/10.1093/nar/15.13.5443 | DOI Listing |
Acta Pharmacol Sin
January 2025
The Fifth Affiliated Hospital, Guangdong Province & NMPA & State Key Laboratory, School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, 511436, China.
Vascular smooth muscle cell (VSMC) phenotypic switching plays a crucial role in the initiation and progression of atherosclerosis. Dehydrocorydaline (DHC), a major active component of the traditional Chinese herbal medicine Rhizoma Corydalis, exhibits diverse pharmacological effects. However, its impact on VSMCs remains largely unknown.
View Article and Find Full Text PDFFASEB J
January 2025
Laboratory of Molecular Pharmacology, Biosignal Research Center, Kobe University, Kobe, Japan.
DFNA1 (deafness, nonsyndromic autosomal dominant 1), initially identified as nonsyndromic sensorineural hearing loss, has been associated with an additional symptom: macrothrombocytopenia. However, the timing of the onset of hearing loss (HL) and thrombocytopenia has not been investigated, leaving it unclear which occurs earlier. Here, we generated a knock-in (KI) DFNA1 mouse model, diaphanous-related formin 1 (DIA1), in which Aequorea coerulescens green fluorescent protein (AcGFP)-tagged human DIA1(p.
View Article and Find Full Text PDFScand J Med Sci Sports
January 2025
Department of Sports Science and Clinical Biomechanics, University of Southern Denmark, Odense, Denmark.
While acute exercise affects sarcoplasmic reticulum (SR) function, the impact of resistance training remains unclear. The purpose of the present study was to investigate SR Ca handling plasticity in response to moderate- and high-volume strength training in elite rowers. Twenty elite male (n = 12) and female (n = 8) rowers performed three weekly strength training sessions for 8 weeks and were randomly allocated to either perform 3 sets (3-SET) or progressive increase from 5 to 10 sets (10-SET) of 10 repetitions during the training period.
View Article and Find Full Text PDFChem Biol Interact
January 2025
Department of Orthopedics, The Affiliated Wuxi Clinical College of Nantong University, Jiangsu, 214000, China. Electronic address:
This study systematically evaluated the toxic effects of fluconazole on the cardiovascular development of zebrafish. Zebrafish embryos were treated with different concentrations of fluconazole (200, 400, and 800 μg/ml) to observe its impact on heart development, reactive oxygen species (ROS) generation, apoptosis, and hemoglobin production. The results showed that as the concentration of fluconazole increased, significant changes in zebrafish heart structure were observed, along with a notable reduction in heart rate.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
January 2025
Department of Biochemistry and Molecular Biology, Dalhousie University, Dalhousie Medicine New Brunswick, 355 Campus Ring Road, Saint John, New Brunswick, E2L 4L5, Canada.
Lipid phosphate phosphatase 3 (LPP3) is a membrane-bound enzyme that hydrolyzes lipid phosphates including the bioactive lipid, lysophosphatidic acid (LPA). Elevated circulating LPA production and cellular LPA signaling are implicated in obesity-induced metabolic and cardiac dysfunction. Deletion of LPP3 in the cardiomyocyte increases circulating LPA levels and causes heart failure and mitochondrial dysfunction in mice.
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