The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.
Activation of protein kinase C inhibits cellular production of the amyloid beta-protein.
Open accessAbstract
The 39-43-amino acid amyloid beta-protein (A beta), which is progressively deposited in cerebral plaques and blood vessels in Alzheimer's disease (AD), is released by cultured human cells during normal metabolism. Here we show that agents which activate protein kinase C or otherwise enhance protein phosphorylation caused a substantial decrease in A beta production in vitro. Protein kinase C activation also markedly decreased A beta release from cells that express mutant forms of the beta-amyloid precursor protein genetically linked to familial AD. Inhibition of A beta secretion could also be effected by direct stimulation of m1 muscarinic acetylcholine receptors with carbachol. These results demonstrate that activation of the protein kinase C signal transduction pathways down-regulates the generation of the amyloidogenic A beta peptide. Pharmacologic agents that activate this system, including a variety of first messengers, could potentially slow the development or growth of some A beta plaques during the early stages of AD.
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Amyloid β-peptide is produced by cultured cells during normal metabolism
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Self-citationIsolation and quantification of soluble Alzheimer's β-peptide from biological fluids
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Cited by
Amyloid Precursor Protein Processing and Alzheimer's Disease
O'Brien, R. J., & Wong, P. C. (2011) · Annual Review of Neuroscience · doi:10.1146/annurev-neuro-061010-113613 · Cited by 2,061
APP processing in Alzheimer’s disease.
Zhang, Y.-W., Thompson, R., Zhang, H., & Xu, H. (2011) · Molecular Brain · doi:10.1186/1756-6606-4-3 · Cited by 983
Lammich, S., Kojro, E., Postina, R., Gilbert, S., Pfeiffer, R., Jasionowski, M., Haass, C., & Fahrenholz, F. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.7.3922 · Cited by 975
Self-citationBuxbaum, J. D., Liu, K.-N., Luo, Y., Slack, J. L., Stocking, K. L., Peschon, J. J., Johnson, R. S., Castner, B. J., Cerretti, D. P., & Black, R. A. (1998) · Journal of Biological Chemistry · doi:10.1074/jbc.273.43.27765 · Cited by 934
The cell biology of β-amyloid precursor protein and presenilin in Alzheimer's disease
Selkoe, D. (1998) · Trends in Cell Biology · doi:10.1016/s0962-8924(98)01363-4 · Cited by 862
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Metadata
- Authors
- Hung, A. Y., Haass, C., Nitsch, R. M., Qiu, W. Q., Citron, M., Wurtman, R. J., Growdon, J. H., & Selkoe, D. J.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 1993-11
- Volume
- 268
- Issue
- 31
- Pages
- 22959-22962
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W1510308646
- Cited by
- 405
- References
- 33
- FWCI
- 15.39
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Hung, A. Y., Haass, C., Nitsch, R. M., Qiu, W. Q., Citron, M., Wurtman, R. J., Growdon, J. H., & Selkoe, D. J. (1993). Activation of protein kinase C inhibits cellular production of the amyloid beta-protein. Journal of Biological Chemistry. https://doi.org/10.1016/s0021-9258(19)49409-x
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