Protein kinase C (PKC) has been implicated in the pathophysiology of Alzheimer's disease (AD). The levels of particular isoforms and the activation of PKC are reduced in postmortem brain cortex of AD subjects. Receptors for activated C kinase (RACK) are a family of proteins involved in anchoring activated PKCs to relevant subcellular compartments. Recent evidence has indicated that the impaired activation (translocation) of PKC in the aging brain is associated with a deficit in RACK1, the most well-characterized member of this family. The present study was conducted to determine whether alterations in RACK1 occurred in cortical areas where an impaired translocation of PKC has been demonstrated in AD. Here we report the presence of RACK1 immunoreactivity in human brain frontal cortex for the first time and demonstrate a decrease in RACK1 content in cytosol and membrane extracts in AD when compared with non-AD controls. By comparison, the levels of the RACK1-related PKC beta II were not modified in the same membrane extracts. These observations add a new perspective in understanding the disease-associated defective PKC signal transduction and indicate that a decrease in an anchoring protein for PKC is an additional determinant of this deficit. (C) 1999 Academic Press.

Battaini F., P.A. (1999). Protein kinase C anchoring deficit in postmortem brains of Alzheimer's disease patients. EXPERIMENTAL NEUROLOGY, 159(2), 559-564 [10.1006/exnr.1999.7151].

Protein kinase C anchoring deficit in postmortem brains of Alzheimer's disease patients

BATTAINI, FIORENZO MARIA;
1999

Abstract

Protein kinase C (PKC) has been implicated in the pathophysiology of Alzheimer's disease (AD). The levels of particular isoforms and the activation of PKC are reduced in postmortem brain cortex of AD subjects. Receptors for activated C kinase (RACK) are a family of proteins involved in anchoring activated PKCs to relevant subcellular compartments. Recent evidence has indicated that the impaired activation (translocation) of PKC in the aging brain is associated with a deficit in RACK1, the most well-characterized member of this family. The present study was conducted to determine whether alterations in RACK1 occurred in cortical areas where an impaired translocation of PKC has been demonstrated in AD. Here we report the presence of RACK1 immunoreactivity in human brain frontal cortex for the first time and demonstrate a decrease in RACK1 content in cytosol and membrane extracts in AD when compared with non-AD controls. By comparison, the levels of the RACK1-related PKC beta II were not modified in the same membrane extracts. These observations add a new perspective in understanding the disease-associated defective PKC signal transduction and indicate that a decrease in an anchoring protein for PKC is an additional determinant of this deficit. (C) 1999 Academic Press.
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore BIO/14
eng
Con Impact Factor ISI
protein kinase c; adult; aged; Alzheimer disease; article; brain cortex; clinical article; controlled study; human; human cell; human tissue; immunoreactivity; pathophysiology; priority journal; signal transduction; Aged; Aged, 80 and over; Alzheimer Disease; Animals; Autopsy; Brain; Cell Membrane; Humans; Isoenzymes; Peptides; Postmortem Changes; Protein Kinase C; Rats; Receptors, Cell Surface; Reference Values
Battaini F., P.A. (1999). Protein kinase C anchoring deficit in postmortem brains of Alzheimer's disease patients. EXPERIMENTAL NEUROLOGY, 159(2), 559-564 [10.1006/exnr.1999.7151].
Battaini, Fm; Pascale, A; Lucchi, L; Pasinetti, Gm; Govoni, S
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2108/51429
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