Protein kinase CK2 is altered in insulin-resistant genetically obese (fa/fa) rats

Nerea Roher, Francesc Miró, Marta José, Ramon Trujillo, Maria Plana, Emilio Itarte

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5 Citations (Scopus)

Abstract

Hepatic insulin receptor levels in 6-week-old obese (fa/fa) rats were about 2-fold lower than those from lean (Fa/-) rats, which agrees with their insulin-resistant state. Nuclear protein kinase CK2 activity and protein content in livers from obese (fa/fa) rats were similar to those of lean (Fa/-) animals but the cytosolic levels were reduced to half, due to a decrease in the 39-kDa catalytic subunit. Marked increases in activity, due to rises in the 44-kDa and 39-kDa catalytic subunits, were seen in the 16 000xg sediments (M1) from insulin-resistant rats, with moderate changes in the 100 000xg sediments (M2). The increase in CK2 binding to M1 did not require increases in the molecular chaperone grp94, which was unaltered in insulin-resistant rats. Copyright (C) 1998 Federation of European Biochemical Societies.
Original languageEnglish
Pages (from-to)211-215
JournalFEBS Letters
Volume437
DOIs
Publication statusPublished - 23 Oct 1998

Keywords

  • Grp94
  • Insulin receptor
  • Insulin resistance
  • Obese (fa/fa) rat
  • Protein kinase CK2
  • Rat liver

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