Events: detail
A knock-in mouse with inactivated ATP binding to CamKII-alpha: The role of CaMKII-mediated phosphorylations in hippocampal function
- Hosted by:
- UCL Department of Anatomy and Developmental Biology
- Speaker:
-
YOKO YAMAGATA, National Institute for Physiological Sciences, Okazaki, JAPAN
- Starts:
- September 10, 2007 at 02:00 pm
- Ends:
- September 10, 2007 at 03:00 pm
- Location:
- University College London Wolfson Institute for Biomedical Research, Cruciform Building, Lecture Theatre 2 (Basement), Gower Street, London, WC1E 6BT United Kingdom
- Maps:
Description
Ca2+/calmodulin-dependent protein kinase II (CaMKII) is abundant in the brain. This enzyme mediates key cellular responses to stimuli, affecting synaptic properties and higher brain function. We have generated the alpha-CamKII (K42R) knock-in mouse. This lysine-to-arginine mutation abolishes ATP binding to alpha-CaMKII, so that substrates can no longer be phosphorylated. Other properties of the enzyme remain intact. I will introduce our findings on the role of CaMKII kinase activity in hippocampal synaptic function, as revealed by electrophysiological and cell biological analyses of the CaMKII-alpha (K42R) knock-in mouse.
- Registration required:
- No
- Free:
- Yes
For more information
- Contact person:
- Jeffrey Vernon, WIBR
- Email:
- j.vernon [ at ] ucl.ac.uk
