Colbran Lab

CaMKII is highly expressed in the brain.  Immunohistochemical approaches have found that it is highly enriched in dendritic spines where it is dynamically associated with postsynaptic densities.  Numerous investigators have reported key roles for CaMKII in regulating many processes in dendritic spines.  Our overarching hypothesis is that functions of CaMKII in spines are modulated by association with CaMKAPs.  The CaMKAPs may function in several ways to modify kinase activity or to colocalize CaMKII with specific subsets of its substrate proteins.  In addition, we have suggested that CaMKII may also function as an autoregulated scaffolding protein that dynamically controls the assembly of complexes containing multiple CaMKAPs.  These multi-CaMKAP complexes may control the trafficking of associated proteins, or may play a role in the dynamic changes in PSD and/or spine morphology.  Our ongoing studies on CaMKII interactions with NMDA receptor subunits, MAGUK proteins, densin and alpha-actinin seek to understand the structural basis for assembly of these complexes, as well as their role in controlling excitatory synaptic transmission.

Use the links below to find our more about our research:

Overview

CaMKII regulation

Striatal signaling in Parkinson's Disease

Feedback regulation of Ca²⁺ channels