An endogenous membrane-bound protein inhibits the phosphorylation of the L-type calcium channel by the cAMP-dependent protein kinase

Woscholski, Ruediger; Marmé, Dieter

doi:10.1016/s0006-291x(05)81589-x

Cited by 1 publication

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“…It has been established that the L-type VDCC is potentiated by PK A (Armstrong and Eckert, 1987;Woscholski and Marme, 1992). Phosphorylation by PKA at two sites on the L-type VDCC increases the probability of channel opening (Sculptoreanu et al, 1993).…”

Section: Role Of Cyclic Amp (Camp) -Dependent Protein Kinase (Pka) I mentioning

confidence: 99%

The Amyloid β‐Protein of Alzheimer's Disease Increases Acetylcholinesterase Expression by Increasing Intracellular Calcium in Embryonal Carcinoma P19 Cells

Sberna

Sáez‐Valero

Beyreuther

et al. 1997

Journal of Neurochemistry

117

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Abstract:One of the characteristic changes that occurs in Alzheimer's disease is the loss of acetylcholinesterase (AChE) from both cholinergic and noncholinergic neurons of the brain. However, AChE activity is increased around amyloid plaques. This increase in AChE may be of significance for therapeutic strategies using AChE inhibitors. The aim of this study was to examine the effect ofamyloid /3-protein (A/3), the major component of amyloid plaques, on AChE expression. A/3 peptides spanning residues 1 -40 or 25-35 increased AChE activity in P19 embryonal carcinoma cells. A peptide containing a scrambled A/3 2535 sequence did not stimulate AChE expression. To examine the possibility that the increase in AChE expression was mediated by an influx of calcium through voltage-dependent calcium channels (VDCCs), drugs acting on VDCCs were tested for their effects. Inhibitors of L-type VDCCs (diltiazem, nifedipine, and verapamil), but not N-or P-or Q-type VDCCs, resulted in a decrease in AChE expression. Agonists of L-type VDCCs (maitotoxin and S(-)-Bay K 8644) increased AChE expression. As L-type VDCCs are known to be modulated by cyclic AMP-dependent protein kinase, the effect of the adenylate cyclase activator forskolin was also examined. Forskolin stimulated AChE expression, an action that was blocked by the L-type VDCC antagonist nifedipine. The A/32535-induced increase in AChE expression was mediated by an L-type VDCC, as the effect was also blocked by nifedipine. The results suggest that the increase in AChE expression around amyloid plaques could be due to a disturbance in calcium homeostasis involving the opening of L-type VDCCs. Key Words: AcetylcholinesteraseAmyloid /3-protein-Voltage-dependent calcium channel-Alzheimer's disease-Cyclic AMP.

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Section: Role Of Cyclic Amp (Camp) -Dependent Protein Kinase (Pka) I mentioning

confidence: 99%

The Amyloid β‐Protein of Alzheimer's Disease Increases Acetylcholinesterase Expression by Increasing Intracellular Calcium in Embryonal Carcinoma P19 Cells

Sberna

Sáez‐Valero

Beyreuther

et al. 1997

Journal of Neurochemistry

117

View full text Add to dashboard Cite

show abstract

An endogenous membrane-bound protein inhibits the phosphorylation of the L-type calcium channel by the cAMP-dependent protein kinase

Cited by 1 publication

References 12 publications

The Amyloid β‐Protein of Alzheimer's Disease Increases Acetylcholinesterase Expression by Increasing Intracellular Calcium in Embryonal Carcinoma P19 Cells

The Amyloid β‐Protein of Alzheimer's Disease Increases Acetylcholinesterase Expression by Increasing Intracellular Calcium in Embryonal Carcinoma P19 Cells

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