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Published online 23 August 2004. doi:10.1083/jcb1665iti3
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 166, Number 5, 607-607
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In This Issue

Calcium lights up cell cycle


Preventing a Ca2+ transient blocks NF-{kappa}B activation and cell cycle entry

Calcium biologists have long suggested that there was a fundamental role for the cation in the cell cycle, but the supporting data have been largely circumstantial. Now, Sée et al. (page 661) have direct evidence for a transient Ca2+ trigger in the initiation of the cell cycle upon serum stimulation. They also find that the transcription factor NF-{kappa}B links the ion flux to a well-known cell cycle control gene, cyclin D1.

Using Ca2+-sensitive dyes, the authors saw that serum-starved fibroblasts responded to serum stimulation with a rise in intracellular Ca2+ that lasted for only 30 s. Serum addition also triggered NF-{kappa}B activation, which is required for cell cycle entry and transcription of cyclin D1, a rate-limiting G1 cyclin.

To determine whether the brief Ca2+ flux was crucial for NF-{kappa}B activation, the investigators introduced a caged Ca2+ scavenger into the cells. Photoactivation of the Ca2+ scavenger prevented the Ca2+ flux that would naturally occur in response to serum stimulation and blocked NF-{kappa}B activity. However, the scavenger was only effective when activated immediately after serum stimulation.

The Ca2+ flux is necessary but not sufficient to induce NF-{kappa}B activity. The researchers find that p42/p44 MAPK activity, which is dependent on both Ca2+ and probably other signals, is also required for NF-{kappa}B activation and cyclin D1 transcription. {blacksquare}



Rabiya Tuma

rabiya{at}nasw.org


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Related Article

Calcium-dependent regulation of the cell cycle via a novel MAPK–NF-{kappa}B pathway in Swiss 3T3 cells
Violaine Sée, Nina K.M. Rajala, David G. Spiller, and Michael R.H. White
J. Cell Biol. 2004 166: 661-672. [Abstract] [Full Text] [PDF]




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