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Showing 1-11 of 11 results for "HPA001349" within Papers
Cai Yuan et al.
Biophysical journal, 118(5), 1058-1066 (2020-01-30)
Detection of the transition between the two myosin isoforms α- and β-myosin in living cardiomyocytes is essential for understanding cardiac physiology and pathology. In this study, the differences in symmetry of polarization spectra obtained from α- and β-myosin in various
Hideshi Niimura et al.
Circulation, 105(4), 446-451 (2002-01-30)
Hypertrophic cardiomyopathy, a familial myocardial condition caused by sarcomere protein mutations, is usually recognized by early adulthood. Hypertrophic cardiomyopathy of the elderly has similar clinical features but, notably, a later age of onset and noncontributory family history. Causes of elderly-onset
Ursula Paula Renó Soci et al.
Clinical science (London, England : 1979), 130(22), 2005-2015 (2016-08-10)
Aerobic exercise-induced cardiac hypertrophy (CH) is a physiological response involving accurate orchestration of gene and protein expression of contractile and metabolic components. The microRNAs: miR-208a, miR-208b and miR-499 are each encoded by a myosin gene and thus are also known
Morihiko Aoyama et al.
Circulation. Heart failure, 9(1), e002081-e002081 (2016-01-02)
Ample evidence demonstrates cardiovascular protection by incretin-based therapy using dipeptidyl peptidase 4 inhibitor (DPP4i) and glucagon-like peptide-1 (GLP-1) under either diabetic or nondiabetic condition. Their action on myocardium is mediated by the cyclic AMP (cAMP) signal; however, the pathway remains
Yung-Hao Ching et al.
Nature genetics, 37(4), 423-428 (2005-03-01)
Atrial septal defect is one of the most common forms of congenital heart malformation. We identified a new locus linked with atrial septal defect on chromosome 14q12 in a large family with dominantly inherited atrial septal defect. The underlying mutation
Vika Smerdu
Journal of anatomy, 243(5), 826-841 (2023-07-08)
To build on the existing data on the pattern of myosin heavy chain (MyHC) isoforms expression in the human muscle spindles, we aimed to verify whether the 'novel' MyHC-15, -2x and -2b isoforms are co-expressed with the other known isoforms
R Matsuoka et al.
American journal of medical genetics, 41(4), 537-547 (1991-12-15)
We have obtained the 5820 nucleotide sequence encoding all 1939 amino acids of the human cardiac alpha-myosin heavy chain (alpha-MHC), as established by dideoxy sequencing of cloned cDNA, genomic DNA and polymerase chain reaction (PCR) amplification products. This sequence represents
Nina Tandon et al.
Journal of tissue engineering and regenerative medicine, 5(6), e115-e125 (2011-05-24)
In vitro application of pulsatile electrical stimulation to neonatal rat cardiomyocytes cultured on polymer scaffolds has been shown to improve the functional assembly of cells into contractile engineered cardiac tissues. However, to date, the conditions of electrical stimulation have not
Charles A Stuart et al.
American journal of physiology. Cell physiology, 310(5), C381-C389 (2015-12-18)
Muscle fiber composition correlates with insulin resistance, and exercise training can increase slow-twitch (type I) fibers and, thereby, mitigate diabetes risk. Human skeletal muscle is made up of three distinct fiber types, but muscle contains many more isoforms of myosin
T A Epp et al.
Genomics, 18(3), 505-509 (1993-12-01)
The human myocardium expresses two cardiac myosin heavy chain (MyHC) isoforms, alpha and beta, that exist in tandem array on chromosome 14q12. We have previously sequenced the entire human cardiac beta-MyHC gene and now report the complete nucleotide sequence of
Elisa Carniel et al.
Circulation, 112(1), 54-59 (2005-07-07)
Mutations in the beta-myosin heavy-chain (betaMyHC) gene cause hypertrophic (HCM) and dilated (DCM) forms of cardiomyopathy. In failing human hearts, downregulation of alphaMyHC mRNA or protein has been correlated with systolic dysfunction. We hypothesized that mutations in alphaMyHC could also
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