The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
A Spatial-Temporal Model of Cell Activation
Abstract
A spatial-temporal model of calcium messenger function is proposed to account for sustained cellular responses to sustained stimuli, as well as for the persistent enhancement of cell responsiveness after removal of a stimulus, that is, cellular memory. According to this model, spatial separation of calcium function contributes to temporal separation of distinct phases of the cellular response. At different cellular sites, within successive temporal domains, the calcium messenger is generated by different mechanisms and has distinct molecular targets. In particular, prolonged cell activation is brought about by the interaction of calcium with another spatially confined messenger, diacylglycerol, to cause the association of protein kinase C with the plasma membrane. Activity of the membrane-associated protein kinase C is controlled by the rate of calcium cycling across the plasma membrane. In some instances, a single stimulus induces both protein kinase C activation and calcium cycling and thus causes prolonged activation; but in others, a close temporal association of distinct stimuli brings about cell activation via interaction of these intracellular messengers. Persistent enhancement of cell responsiveness after removal of stimuli is suggested to be due to the continued association, or anchoring, of protein kinase C to the membrane.
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Citations
Cites
Intracellular injections of EGTA block induction of hippocampal long-term potentiation
Lynch, G., Larson, J., Kelso, S., Barrionuevo, G., & Schottler, F. (1983) · Nature · doi:10.1038/305719a0 · Cited by 1,116
Lai, Y., Nairn, A. C., & Greengard, P. (1986) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.83.12.4253 · Cited by 292
Kojima, I., Kojima, K., & Rasmussen, H. (1985) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)39349-3 · Cited by 142
Cited by
Calcium in Ischemic Cell Death
Kristián, T., & Siesjö, B. K. (1998) · Stroke · doi:10.1161/01.str.29.3.705 · Cited by 825
Huang, Y.-Y., Li, X.-C., & Kandel, E. R. (1994) · Cell · doi:10.1016/0092-8674(94)90401-4 · Cited by 490
Mattson, M., Murrain, M., Guthrie, P., & Kater, S. (1989) · The Journal of Neuroscience · doi:10.1523/jneurosci.09-11-03728.1989 · Cited by 480
Brody, C. D., Romo, R., & Kepecs, A. (2003) · Current Opinion in Neurobiology · doi:10.1016/s0959-4388(03)00050-3 · Cited by 284
Neuronal ELAV proteins enhance mRNA stability by a PKCα-dependent pathway
Pascale, A., Amadio, M., Scapagnini, G., Lanni, C., Racchi, M., Provenzani, A., Govoni, S., Alkon, D. L., & Quattrone, A. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0504702102 · Cited by 129
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Metadata
- Authors
- Alkon, D. L., & Rasmussen, H.
- Venue
- Science
- Published
- 1988-02-26
- Volume
- 239
- Issue
- 4843
- Pages
- 998-1005
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2068270309
- Cited by
- 342
- References
- 3
- FWCI
- 19.31
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
