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Charles E. Murry

Researcher at University of Washington

Publications -  290
Citations -  46975

Charles E. Murry is an academic researcher from University of Washington. The author has contributed to research in topics: Induced pluripotent stem cell & Stem cell. The author has an hindex of 85, co-authored 270 publications receiving 43033 citations. Previous affiliations of Charles E. Murry include Duke University & Fred Hutchinson Cancer Research Center.

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Tunable electroconductive decellularized extracellular matrix hydrogels for engineering human cardiac microphysiological systems

TL;DR: In this paper, a hybrid hydrogel comprised of decellularized porcine myocardial extracellular matrix (dECM) and reduced graphene oxide (rGO) was developed to provide a more instructive microenvironment for proper cell and tissue development.
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Targeted genomic integration of a selectable floxed dual fluorescence reporter in human embryonic stem cells.

TL;DR: Zinc finger nuclease technology is used to stably insert a unique, selectable, floxed dual-fluorescence reporter transgene into the AAVS1 locus of RUES2 hESCs, a useful new tool for both in vitro fate mapping studies and the selection of useful differentiated cell types.
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Monocyte Chemoattractant Protein 1–Mediated Migration of Mesenchymal Stem Cells Is a Source of Intimal Hyperplasia

TL;DR: The adventitia is a potentially important cellular source that contributes to intimal hyperplasia, and MCP-1 is a potent chemokine for the recruitment of adventitial vascular progenitor cells to intima lesions.
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Quantitative proteomics identify DAB2 as a cardiac developmental regulator that inhibits WNT/β-catenin signaling

TL;DR: This work reveals a regulator of cardiac development, Disabled 2, and found that in zebrafish embryos, it negatively regulates WNT/β-catenin signaling to promote cardiomyocyte differentiation, revealing a highly conserved, previously unidentified process relevant for human heart development.
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Transgenic overexpression of ribonucleotide reductase improves cardiac performance

TL;DR: Long-term elevation of cardiac [dATP] results in sustained elevation of basal left ventricular performance, with maintained β-adrenergic responsiveness and energetic reserves, and is concluded that this occurs primarily via enhanced myofilament activation and contraction.