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Protein kinase CK2 is altered in insulin‐resistant genetically obese ( fa/fa ) rats
Author(s) -
Roher Nerea,
Miró Francesc,
José Marta,
Trujillo Ramon,
Plana Maria,
Itarte Emilio
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)01230-7
Subject(s) - medicine , endocrinology , insulin , cytosol , protein subunit , insulin receptor , chemistry , protein kinase a , receptor , insulin resistance , kinase , biology , enzyme , biochemistry , gene
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 16 000× g sediments (M1) from insulin‐resistant rats, with moderate changes in the 100 000× g 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.