Kinetics of the translocation and phosphorylation of B-crystallin in mouse heart mitochondria during ex vivo ischemia
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[PDF] [Full Text] [Abstract] , December , 2009; 50 (12): 5559-5566. IOVS Sindhu Saraswathy and Narsing A. Rao Mitochondrial Proteomics in Experimental Autoimmune Uveitis Oxidative Stress [PDF] [Full Text] [Abstract] , October 26, 2010; 107 (43): 18481-18486. PNAS O. Gramolini Anthony Peter H. Backx, Peter Liu, Thomas Kislinger, David H. MacLennan, Andrew Emili and Nicolas Bousette, Shaan Chugh, Vincent Fong, Ruth Isserlin, Kyoung-Han Kim, Allen Volchuk, -crystallin-B α against apoptosis that is mediated by Constitutively active calcineurin induces cardiac endoplasmic reticulum stress and protects [PDF] [Full Text] [Abstract] , December 9, 2011; 109 (12): 1354-1362. Circulation Research Shikha Mishra, Charles B.B. Gray, Shigeki Miyamoto, Donald M. Bers and Joan Heller Brown Location Matters : Clarifying the Concept of Nuclear and Cytosolic CaMKII Subtypes
منابع مشابه
Kinetics of the translocation and phosphorylation of alphaB-crystallin in mouse heart mitochondria during ex vivo ischemia.
alphaB-crystallin (alphaBC) is a small heat shock protein expressed at high levels in the myocardium where it protects from ischemia-reperfusion damage. Ischemia-reperfusion activates p38 MAP kinase, leading to the phosphorylation of alphaBC on serine 59 (P-alphaBC-S59), enhancing its ability to protect myocardial cells from damage. In the heart, ischemia-reperfusion also causes the translocati...
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متن کاملLocalization of phosphorylated alphaB-crystallin to heart mitochondria during ischemia-reperfusion.
The cytosolic small heat shock protein alphaB-crystallin (alphaBC) is a molecular chaperone expressed in large quantities in the heart, where it protects from stresses such as ischemia-reperfusion (I/R). Upon I/R, p38 MAP kinase activation leads to phosphorylation of alphaBC on Ser(59) (P-alphaBC-S59), which increases its protective ability. alphaBC confers protection, in part, by interacting w...
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BACKGROUND We have recently shown that postischemic administration of intralipid protects the heart against ischemia-reperfusion injury. Here we compared the cardioprotective effects of intralipid with cyclosporine-A, a potent inhibitor of the mitochondrial permeability transition pore opening. METHODS In vivo rat hearts or isolated Langendorff-perfused mouse hearts were subjected to ischemia...
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