Targeting proteasome worsens atherosclerosis.
نویسنده
چکیده
957 Letter to the Editor Nonbone Marrow–Derived Endothelial Progenitor Cells: What Is Their Exact Location? Alexandra Aicher, Stefanie Dimmeler, Christopher Heeschen Web Site Feature e102 On the cover: The image shows on the left the formation of the pulmonary myocardial sleeves by rapid proliferation of the just-differentiated myocardium (section of an E12.5 embryo stained for BrdU (red), cTnI (blue) and sytoxgreen (green)). On the right is a 3D reconstruction of an E14.5 wild type heart showing the forming pulmonary myocardial sleeve (grey, Nkx2-5-positive myocardium; aqua, Nkx2-5-negative myocardium; red, lumen pulmonary vein; orange, lumen caval veins). See related article, page 902. by gest on M ay 1, 2017 http://circhajournals.org/ D ow nladed from
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The ubiquitin-proteasome pathway is the principal mechanism for the turnover of short-lived proteins in eukaryotic cells. In this pathway, the covalent ligation of ubiquitin to the substrate is a signal for recognition by the 26S proteasome. Recent studies indicate that targeting of substrates of the ubiquitin pathway to the proteasome is usually accomplished by the ligation of a polyubiquitin ...
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ورودعنوان ژورنال:
- Circulation research
دوره 101 9 شماره
صفحات -
تاریخ انتشار 2007