作者: V Nivet , P.J Antoine , M Amessou , G Descamps , B Desbuquois
DOI: 10.1016/S0303-7207(98)00155-5
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摘要: Abstract Ca 2+ -dependent protein kinase C (cPKC) activity and expression have been studied in livers from hypoinsulinemic streptozotocin (STZ)-induced diabetic untreated control rats. In rats, cPKC was slightly decreased liver total particulate nuclear fractions but unchanged mitochondrial-lysosomal, microsomal cytosolic fractions. On Western immunoblot analysis, PKC α identified as two distinct proteins of 90 81 kDa. the abundance kDa increased most subcellular with a maximun (180%) that unchanged. β 2 detected single levels Liver mRNA measured by reverse transcription competitive PCR amplification were similar The rats reversed insulin not phlorizin, suggesting it did result hyperglycemia. We conclude STZ-induced diabetes induces biologically inactive form which differs active an undefined post-translational modification, possibly increase phosphorylation state.