Refinement of dendrites occurs in response to stimulation which causes Ca2+ influx through voltage-sensitive Ca2+ channels and activates downstream signaling pathways. As a result, local cytoskeletal rearrangements are triggered, as well as transcription-dependent global dendritic remodeling. The latter mechanism involves a number of transcriptional factors including cAMP-responsive element binding protein (CREB), CREB-binding protein (CBP) and NeuroD (Redmond et al., 2002). The nBAF component CREST is a calcium-sensitive transcriptional coactivator which itself does not bind DNA but interacts with CREB to actuate transcriptional outcome (Aizawa et al., 2004). While CREST-null mice are viable, they exhibit dendritic defects in the cortex and the hippocampus similar to a BAF53b-null (Aizawa et al., 2004). The proper localization of the CREST-containing nBAF complex at key target promoters, including Ephexin1, requires BAF53b, although BAF53b is not necessary for the assembly of nBAF (Wu et al., 2007).
