ArticleProceedings of the National Academy of Sciences of the United States of America1994
Ca2+ triggers premature inactivation of the cdc2 protein kinase in permeabilized sea urchin embryos.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 19 citations in OpenAlex.
- Activation of protein kinase C alters p34(cdc2) phosphorylation state and kinase activity in early sea urchin embryos by abolishing intracellular Ca2+ transients.The Biochemical journal · 2000Article
- The coordination of centrosome reproduction with nuclear events of the cell cycle in the sea urchin zygote.The Journal of cell biology · 1998Article
- Characterization of N-ethylmaleimide-sensitive thiol groups required for the GTP-dependent fusion of endoplasmic reticulum membranes.The Biochemical journal · 1995Article
- Nuclear envelope breakdown is under nuclear not cytoplasmic control in sea urchin zygotes.The Journal of cell biology · 1995Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exit from mitosis requires inactivation of the cyclin B-p34cdc2 protein kinase complex. Since increased cytosolic Ca2+ has been implicated as a potential trigger of mitotic progression, we directly tested the possibility that Ca2+ triggers the pathway responsible for inactivating the cdc2 kinase, using sea urchin embryos permeabilized at various stages of the cell cycle. In cells permeabilized during late interphase and prophase, micromolar Ca2+ induced premature inactivation of the cdc2 kinase without affecting the absolute amount of p34cdc2 protein. Inactivation was selective for the cdc2 kinase, as elevated Ca2+ had no effect on cAMP-dependent protein kinase activity. Premature cdc2 kinase inactivation did not require cyclin B destruction, but did coincide with the dissociation of cyclin B-p34cdc2 complexes. In cells permeabilized during prometaphase and metaphase, cdc2 kinase inactivation was Ca(2+)-independent, presumably because at these later times the inactivating pathway had been enabled prior to permeabilization. This work provides evidence that Ca2+ is the physiological trigger enabling cdc2 kinase inactivation during mitosis.
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