Found: 19
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Coronary arterial vasculature in the pathophysiology of hypertrophic cardiomyopathy.
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- Pflügers Archiv: European Journal of Physiology, 2019, v. 471, n. 5, p. 769, doi. 10.1007/s00424-018-2224-y
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- Article
The role of tropomyosin in the regulation of myocardial contraction and relaxation.
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- Pflügers Archiv: European Journal of Physiology, 2003, v. 446, n. 1, p. 1, doi. 10.1007/s00424-002-0900-3
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- Article
Altered coronary artery function, arteriogenesis and endothelial YAP signaling in postnatal hypertrophic cardiomyopathy.
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- Frontiers in Physiology, 2023, v. 14, p. 1, doi. 10.3389/fphys.2023.1136852
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- Article
Truncation of the N-terminus of cardiac troponin I initiates adaptive remodeling of the myocardial proteosome via phosphorylation of mechano-sensitive signaling pathways.
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- Molecular & Cellular Biochemistry, 2022, v. 477, n. 6, p. 1803, doi. 10.1007/s11010-022-04414-3
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- Article
Troponin I in the murine myocardium: influence on length-dependent activation and interfilament spacing.
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- Journal of Physiology, 2003, v. 547, n. 3, p. 951, doi. 10.1111/j.1469-7793.2003.00951.x
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- Article
Expression of slow skeletal troponin I in adult transgenic mouse heart muscle reduces the force decline observed during acidic conditions.
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- Journal of Physiology, 2001, v. 536, n. 3, p. 863, doi. 10.1111/j.1469-7793.2001.00863.x
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- Article
Three‐dimensional spatial quantitative analysis of cardiac lymphatics in the mouse heart.
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- Microcirculation, 2023, v. 30, n. 7, p. 1, doi. 10.1111/micc.12826
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- Article
Cardiac-Specific Expression of the Tetracycline Transactivator Confers Increased Heart Function and Survival Following Ischemia Reperfusion Injury.
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- PLoS ONE, 2012, v. 7, n. 1, p. 1, doi. 10.1371/journal.pone.0030129
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- Article
Ceramide-mediated depression in cardiomyocyte contractility through PKC activation and modulation of myofilament protein phosphorylation.
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- Basic Research in Cardiology, 2014, v. 109, n. 6, p. 1, doi. 10.1007/s00395-014-0445-6
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Differential effects of isoflurane and ketamine/inactin anesthesia on cAMP and cardiac function in FVB/N mice during basal state and ß-adrenergic stimulation.
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- Basic Research in Cardiology, 2005, v. 100, n. 2, p. 147, doi. 10.1007/s00395-004-0503-6
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- Article
B-arrestin-2 Signaling Is Important to Preserve Cardiac Function During Aging.
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- Frontiers in Physiology, 2021, v. 12, p. 1, doi. 10.3389/fphys.2021.696852
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- Article
Modifications of Sarcoplasmic Reticulum Function Prevent Progression of Sarcomere-Linked Hypertrophic Cardiomyopathy Despite a Persistent Increase in Myofilament Calcium Response.
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- Frontiers in Physiology, 2020, p. 1, doi. 10.3389/fphys.2020.00107
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- Article
Emerging Concepts of Mechanisms Controlling Cardiac Tension: Focus on Familial Dilated Cardiomyopathy (DCM) and Sarcomere-Directed Therapies.
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- Biomedicines, 2024, v. 12, n. 5, p. 999, doi. 10.3390/biomedicines12050999
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- Article
Early sensitization of myofilaments to Ca<sup>2+</sup> prevents genetically linked dilated cardiomyopathy inmice.
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- Cardiovascular Research, 2017, v. 113, n. 8, p. 915, doi. 10.1093/cvr/cvx068
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- Article
Knockout of p21-activated kinase-1 attenuates exercise-induced cardiac remodelling through altered calcineurin signalling.
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- Cardiovascular Research, 2015, v. 108, n. 3, p. 335, doi. 10.1093/cvr/cvv234
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- Article
Cardiac myosin light chain phosphorylation and inotropic effects of a biased ligand, TRV120023, in a dilated cardiomyopathy model.
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- Cardiovascular Research, 2015, v. 107, n. 2, p. 226, doi. 10.1093/cvr/cvv162
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- Article
Troponin I phosphorylation plays an important role in the relaxant effect of β-adrenergic stimulation in mouse hearts
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- Cardiovascular Research, 2004, v. 61, n. 4, p. 756, doi. 10.1016/j.cardiores.2003.12.019
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- Article
Negative inotropic mechanisms of β-cardiotoxin in cardiomyocytes by depression of myofilament ATPase activity without activation of the classical β-adrenergic pathway.
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- Scientific Reports, 2021, v. 11, n. 1, p. 1, doi. 10.1038/s41598-021-00282-x
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Impaired cardiomyocyte relaxation and diastolic function in transgenic mice expressing slow skeletal troponin I in the heart.
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- Journal of Physiology, 1999, v. 517, n. 1, p. 143, doi. 10.1111/j.1469-7793.1999.0143z.x
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- Article