Shock Protein 27 Mutant Protects Against Ischemia/Reperfusion Injury in a Transgenic Overexpression of Wild-Type Heat Shock Protein 27 and a Nonphosphorylatable Heat
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چکیده
John M. Hollander, Jody L. Martin, Darrell D. Belke, Brian T. Scott, Eric Swanson, Vignesh Mouse Model Shock Protein 27 Mutant Protects Against Ischemia/Reperfusion Injury in a Transgenic Overexpression of Wild-Type Heat Shock Protein 27 and a Nonphosphorylatable Heat Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 2004 American Heart Association, Inc. All rights reserved. is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Circulation doi: 10.1161/01.CIR.0000148825.99184.5
منابع مشابه
Overexpression of wild-type heat shock protein 27 and a nonphosphorylatable heat shock protein 27 mutant protects against ischemia/reperfusion injury in a transgenic mouse model.
BACKGROUND The small heat shock protein 27 (hsp27) increases in expression with ischemia/reperfusion (I/R) insult in the heart. One feature of the small hsps is their ability to oligomerize and form intracellular aggregates. Oligomerization pattern is governed by the phosphorylation state of the protein that may influence their ability to protect against cellular stresses. METHODS AND RESULTS...
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