Myocyte protection by 10 kD heat shock protein (Hsp10) involves the mobile loop and attenuation of the Ras GTP-ase pathway

摘要: Heat shock proteins (hsp), hsp60 and hsp10, are involved in the folding of imported mitochondrial refolding denatured after stress. We examined whether hsp10 can reduce myocyte death by its function or interacting with cytoplasmic signaling pathways. Overexpression adenoviral infection decreased induced hydrogen peroxide, sodium cyanide, simulated ischemia reoxygenation (SI/RO). generated an vector coding for a temperature-sensitive mutant protein (P34H), incapable cooperatively malate dehydrogenase hsp60. potentiated SI/RO-induced death. Analysis electron transport chain revealed increased Complex I capacity overexpression, whereas hsp10(P34H) overexpression II capacity. Hsp10 preserved both SI/RO. Examination Ras GTP-ase pathway indicated that inhibition was required protection hsp10. Constitutive activation abolished effects afforded hsp10(P34H). inactivated Raf, ERK, p90Ribosomal kinase (p90RSK) before Our results suggest complex mechanisms against This mechanism may involve mobile loop attenuation pathway.