Active Ca2+ channels, according to Hudmon et al. (page 537), get their own dedicated Ca2+ sensors that cause well-used channels to open with gusto.
Some Ca2+ channels, including voltage-gated L-type channels, let through more Ca2+ per opening when they are used frequently. This positive feedback, known as facilitation, allows fast-beating cardiac cells, for instance, to beat harder (as during exercise). The new findings reveal that local retention of a Ca2+/calmodulin-dependent kinase, CaMKII, is behind this ability.
CaMKII is activated by autophosphorylation in response to Ca2+/calmodulin. The authors find that CaMKII then tethers itself to the pore-forming α1C subunit of the L-type channel, which is abundant in heart muscle. Even upon dephosphorylation, CaMKII lingers at the channel.
From this position, the kinase can up-regulate channel activity when Ca2+ influx is frequent. The authors show...
