ArticleProceedings of the National Academy of Sciences of the United States of America1998
Alzheimer's-specific effects of soluble beta-amyloid on protein kinase C-alpha and -gamma degradation in human fibroblasts.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 76 citations in OpenAlex.
- Morphometric imaging biomarker identifies Alzheimer's disease even among mixed dementia patients.Scientific reports · 2022Trial
- The roles of RACK1 in the pathogenesis of Alzheimer's disease.Journal of biomedical research · 2024Article
- Bryostatin-1: a promising compound for neurological disorders.Frontiers in pharmacology · 2023Review
- Mechanistic insight of the potential of geraniol against Alzheimer's disease.European journal of medical research · 2022Article
- The Implication of Androgens in the Presence of Protein Kinase C to Repair Alzheimer’s Disease-Induced Cognitive DysfunctionIranian biomedical journal · 2020Review
- Heat shock proteins regulate activation-induced proteasomal degradation of the mature phosphorylated form of protein kinase C.The Journal of biological chemistry · 2013Article
- Agonist-induced down-regulation of endogenous protein kinase c α through an endolysosomal mechanism.The Journal of biological chemistry · 2013Article
- Apolipoprotein E3 (ApoE3) but not ApoE4 protects against synaptic loss through increased expression of protein kinase C epsilon.The Journal of biological chemistry · 2012Article
- Relationships between the amyloid precursor protein and its various proteolytic fragments and neuronal systems.Alzheimer's research & therapy · 2012Article
- Synaptic protein alterations in Parkinson's disease.Molecular neurobiology · 2012Review
- Evaluation of systemic administration of Boswellia papyrifera extracts on spatial memory retention in male rats.Journal of natural medicines · 2011Article
- PKC ε activation prevents synaptic loss, Aβ elevation, and cognitive deficits in Alzheimer's disease transgenic mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Identification of novel small molecule activators of nuclear factor-κB with neuroprotective action via high-throughput screening.Journal of neuroscience research · 2011Article
- Natural products as a source of Alzheimer's drug leads.Natural product reports · 2011Review
- Calcium induces expression of cytoplasmic gelsolin in SH-SY5Y and HEK-293 cells.Neurochemical research · 2010Article
- A cellular model of Alzheimer's disease therapeutic efficacy: PKC activation reverses Abeta-induced biomarker abnormality on cultured fibroblasts.Neurobiology of disease · 2009Article
- An internally controlled peripheral biomarker for Alzheimer's disease: Erk1 and Erk2 responses to the inflammatory signal bradykinin.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Bryostatin-1: pharmacology and therapeutic potential as a CNS drug.CNS drug reviews · 2006Review
- Activation of glycogen synthase kinase-3 induces Alzheimer-like tau hyperphosphorylation in rat hippocampus slices in culture.Journal of neural transmission (Vienna, Austria : 1996) · 2006Article
- Therapeutic effects of PKC activators in Alzheimer's disease transgenic mice.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a multifactorial disease in which beta-amyloid peptide (betaAP) plays a critical role. We report here that the soluble fraction 1-40 of betaAP differentially degrades protein kinase C-alpha and -gamma (PKCalpha and PKCgamma) isoenzymes in normal (age-matched controls, AC) and AD fibroblasts most likely through proteolytic cascades. Treatment with nanomolar concentrations of betaAP(1-40) induced a 75% decrease in PKCalpha, but not PKCgamma, immunoreactivity in AC fibroblasts. In the AD fibroblasts, a 70% reduction of the PKCgamma, but not PKCalpha, immunoreactivity was observed after betaAP treatment. Preincubation of AC or AD fibroblasts with 50 microM lactacystine, a selective proteasome inhibitor, prevented beta-AP(1-40)-mediated degradation of PKCalpha in the AC cells, and PKCgamma in the AD fibroblasts. The effects of betaAP(1-40) on PKCalpha in AC fibroblasts were prevented by inhibition of protein synthesis and reversed by PKC activation. A 3-hr treatment with 100 nM phorbol 12-myristate 13-acetate restored the PKCalpha signal in treated AC cells but it did not reverse the effects of betaAP(1-40) on PKCgamma in the AD fibroblasts. Pretreatment with the protein synthesis inhibitor, cycloheximide (CHX, 100 microM), inhibited the effects of betaAP(1-40) on PKCalpha and blocked the rescue effect of phorbol 12-myristate 13-acetate in AC fibroblasts but did not modify PKCgamma immunoreactivity in AD cells. These results suggest that betaAP(1-40) differentially affects PKC regulation in AC and AD cells via proteolytic degradation and that PKC activation exerts a protective role via de novo protein synthesis in normal but not AD cells.
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