Meeting details menu

Meeting Authors
Meeting Abstracts
Keynote lectures
Oral communications
Poster presentations
Special symposia
Other

Acta Physiologica Congress

Back

Acta Physiologica 2007; Volume 189, Supplement 653
The 86th Annual Meeting of The German Physiological Society
3/25/2007-3/28/2007
Hannover, Germany


TRANSREGULATION OF KINETICS OF CALCIUM CALMODULIN KINASE II (CAMKII) IS IMPLICATED IN ANTI-APOPTOTIC CONTROL
Abstract number: O20-5

Fahrmann1 M, Honisch1 S, Kaufhold1 MA, Leitges1 M, Beil1 W

1Medizinische Hochschule Hannover, Institut fr Pharmakologie

Application of PP1/PP2B inhibitors revealed implication of CaMKII in apoptosis. Physiological relevance and mechanism of CaMKII-triggered apoptosis, however, remains largely unclear. Here we suggest that stringent tuning of activity regulating phosphorylations of CaMKII at T286/287 and T305/306 protects cells from long-term hyperactivity and, therefore, increased rate of apoptosis. Calcium-induced kinetics of tubulovesicular CaMKII showed a rapid but transient increase of hyperphosphorylation at T286/287 and T305/306 which reached a peak after 7 min. Hyperphosphorylation was rapidly followed by a half lower but constant level of phosphorylation designated adaptation. Disturbance of CaMKII transregulation by the PP1/PP2A-inhibitor calyculin A resulted in long-term (>20 min) hyperphosphorylation of T286/287 as well as T305/306, and strongly correlated with an increased rate of apoptosis. Adaptation of phosphorylation at T286/287 failed if phosphatases PP1, PP2A, PP2B or PKC-a were either pharmacologically blocked, or, in the case of PKC-a, were knocked out in mice. In contrast, secretory membrane-associated, autonomous CaMKII was, remarkably robust towards regulations by PP1, PP2A, PP2B or PKC-a. In conclusion, if adaptation failed CaMKII became long-term hyperactive for more than 20 min which seemed to be sufficient to trigger apoptosis.

To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 189, Supplement 653 :O20-5

Our site uses cookies to improve your experience.You can find out more about our use of cookies in our standard cookie policy, including instructions on how to reject and delete cookies if you wish to do so.

By continuing to browse this site you agree to us using cookies as described in our standard cookie policy .

CLOSE