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.

@article{Hollander2004OverexpressionOW,
  title={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.},
  author={John Hollander and Jody L Martin and Darrell D. Belke and Brian T. Scott and Eric A Swanson and Vignesh Prasad Krishnamoorthy and Wolfgang H. Dillmann},
  journal={Circulation},
  year={2004},
  volume={110 23},
  pages={3544-52}
}
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 We generated transgenic (tg) mice that overexpress a wild-type human hsp27 (hsp27tg) protein or a… CONTINUE READING

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