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Functional Impairment in Protein Kinase C by RACK1 (Receptor for Activated C Kinase 1) Deficiency in Aged Rat Brain Cortex
Author(s) -
Pascale Alessia,
Fortino Ida,
Govoni Stefano,
Trabucchi Marco,
Wetsel William C.,
Battaini Fiorenzo
Publication year - 1996
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1996.67062471.x
Subject(s) - protein kinase c , chromosomal translocation , receptor , microbiology and biotechnology , biology , kinase , cortex (anatomy) , calcium , signal transduction , medicine , neuroscience , chemistry , endocrinology , biochemistry , gene
Several laboratories have reported a lack of protein kinase C (PKC) activation in response to various stimuli in the brain of aged rats. It has been suggested that changes in lipid membrane composition could be related to this functional deficit. However, recent evidence has indicated that the translocation of PKC to the different subcellular compartments is controlled by protein‐protein interactions. Recently, a class of proteins, termed receptors for activated C kinase (RACKs), have been described that bind PKC. The present study was conducted to determine whether alterations in RACK1, the best‐characterized member of RACKs, were associated with changes in translocation and expression of PKC. Quantitative immunoblotting revealed that RACK1 content was decreased by ∼50% in aged rat brain cortex, compared with that in adult and middle‐aged animals. The levels of calcium‐independent PKCδ and ε, interacting with RACK1, and related calcium‐independent PKC activity were not modified by the aging process. By comparison, phorbol ester‐stimulated translocation of this activity and of PKCδ and ε immunoreactivity was absent in cortex from aged animals, as well as the translocation of the calcium‐dependent PKCβ, also known to interact with RACK1. These results indicate that a deficit in RACK1 may contribute to the functional impairment in PKC activation observed in aged rat brain.