Hanna Osinska9
James Gulick7
Jeffery D Molkentin3
9Hanna Osinska
7James Gulick
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In response to numerous pathologic stimuli, the myocardium undergoes a hypertrophic response characterized by increased myocardial cell size and activation of fetal cardiac genes. We show that cardiac hypertrophy is induced by the calcium-dependent phosphatase calcineurin, which dephosphorylates the transcription factor NF-AT3, enabling it to translocate to(More)
Sudden cardiac death exhibits diurnal variation in both acquired and hereditary forms of heart disease, but the molecular basis of this variation is unknown. A common mechanism that underlies susceptibility to ventricular arrhythmias is abnormalities in the duration (for example, short or long QT syndromes and heart failure) or pattern (for example,(More)
BACKGROUND Transgenic and gene-targeted models have focused on the mouse. Fundamental differences between the mouse and human exist in Ca2+ handling during contraction/relaxation and in alterations in Ca2+ flux during heart failure, with the rabbit more accurately reflecting the human system. METHODS AND RESULTS Cardiac troponin I (cTnI) mutations can(More)
  • Patrick C H Hsieh, Vincent F M Segers, Michael E Davis, Catherine MacGillivray, Joseph Gannon, Jeffery D Molkentin +2 others
  • 2007
An emerging concept is that the mammalian myocardium has the potential to regenerate, but that regeneration might be too inefficient to repair the extensive myocardial injury that is typical of human disease. However, the degree to which stem cells or precursor cells contribute to the renewal of adult mammalian cardiomyocytes remains controversial. Here we(More)
As the world market for telecommunications underwent a massive downturn in the early 2000s, Motorola, Inc. needed to cut costs and increase productivity throughout its operations. It had to identify a method of reducing the time and effort required to prepare for and conduct negotiations with its suppliers, simplify their coordination , and optimize(More)
  • Jeffrey M. Lynch, Marjorie Maillet, Davy Vanhoutte, Aryn Schloemer, Michelle A. Sargent, N. Scott Blair +10 others
  • 2012
Thrombospondin (Thbs) proteins are induced in sites of tissue damage or active remodeling. The endoplasmic reticulum (ER) stress response is also prominently induced with disease where it regulates protein production and resolution of misfolded proteins. Here we describe a function for Thbs as ER-resident effectors of an adaptive ER stress response. Thbs4(More)
  • Michael J. Previs, Benjamin L. Prosser, Ji Young Mun, Samantha Beck Previs, James Gulick, Kyounghwan Lee +4 others
  • 2015
This PDF file includes: Fig. S1. Two-color dSTORM super-resolution imaging of MyBP-C and ryanodine receptors (RyR2). Fig. S2. Treatment with the contractile inhibitor blebbistatin does not obscure sarcomeric calcium gradients. Fig. S3. Calcium-dependent regulation of native thin filament motion. Fig. S4. Histograms for thin filaments on(More)
We tested whether cardiac myosin binding protein-C (cMyBP-C) affects myosin cross-bridge kinetics in the two cardiac myosin heavy chain (MyHC) isoforms. Mice lacking cMyBP-C (t/t) and transgenic controls $$( {\text{WT}}^{\text{t/t}} )$$ ( WT t/t ) were fed l-thyroxine (T4) to induce 90/10 % expression of α/β-MyHC. Non-transgenic (NTG) and t/t mice were fed(More)
Cardiac myosin binding protein-C (cMyBP-C), a sarcomeric protein with 11 domains, C0–C10, binds to the myosin rod via its C-terminus, while its N-terminus binds regions of the myosin head and actin. These N-terminal interactions can be attenuated by phosphorylation of serines in the C1–C2 motif linker. Within the sarcomere, cMyBP-C exists in a range of(More)
Calcineurin is a protein phosphatase that is uniquely regulated by sustained increases in intracellular Ca(2+) following signal transduction events. Calcineurin controls cellular proliferation, differentiation, apoptosis, and inducible gene expression following stress and neuroendocrine stimulation. In the adult heart, calcineurin regulates hypertrophic(More)