Cardioprotection mediated by urocortin is dependent on PKCε activation K. M. Lawrence * ,1 , A. M. N. Kabir † , M. Bellahcene † , S. Davidson * , X. B. Cao † , J. McCormick * , R. A. Mesquita † , C. J. Carroll * , A. Chanalaris * , P. A. Townsend * , M. Hubank * , A. Stephanou * , R. A. Knight ‡ , M. S. Marber † and D. S. Latchman * * Medical Molecular Biology Unit, Institute of Child Health, University College, London; † The Rayne Institute, St. Thomas’s Hospital, London; and ‡ National Heart and Lung Institute, Royal Brompton Hospital, London, UK 1 Correspondence: Medical Molecular Biology Unit, Institute of Child Health, University College, 30 Guilford St., London WC1N 1EH, UK. E-mail:k.lawrence@ich.ucl.ac.uk <h3>SPECIFIC AIMS</h3> Urocortin (Ucn) is an endogenous cardioprotective agent that protects against the damaging effects of ischemia and reperfusion injury in vitro and in vivo. The mechanism of action of Ucn involves acute activation of target molecules and, as revealed using affymetrix gene chip technology, altered gene expression of different end effector molecules. Here we report an increase in mRNA and protein levels of protein kinase C
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Cardioprotection mediated by urocortin is dependent on PKCε activation
Lawrence, K. M.; Kabir, A. M. N.; Bellahcene, M.; Davidson, S.; Cao, X. B.; McCormick, J.; Mesquita, R. A.; Carroll, C. J.; Chanalaris, A.; Townsend, P. A.; Hubank, M.; Stephanou, A.; Knight, R. A.; Marber, M. S.; Latchman, D. S.
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, Volume 19 (7): 831
Fed of American Socs for Experimental Biology – May 1, 2005
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