TRPC

TRPC is a family of transient receptor potential cation channels in animals.

TRPC channels form the subfamily of channels in human most closely related to drosophila TRP channels. In terms of structure, this family possesses a number of similar characteristics. At the proximal C-terminus of this sub-family is a TRP box motif containing the invariant EWKFAR sequence and between 3 and 4 ankyrin repeats near the N-terminus. These channels are non-selectively permeable to cations, with a selectivity of calcium over sodium variable among the different members. Many of TRPC channel subunits are able to coassemble. The predominant TRPC channels in the mammalian brain are the TRPC 1,4 and 5 and they are densely expressed in corticolimbic brain regions, like the hippocampus, prefrontal cortex and lateral septum. The TRPC channels 1,4 and 5 functional group is activated by the metabotropic glutamate receptor group 1 agonist DHPG.

In general, TRPC channels can be activated by phospholipase C stimulation, with some members also activated by diacylglycerol. There is one at least one report that TRPC1 is also activated by stretching of the membrane and TRPC5 channels are activated by extracellular reduced thioredoxin.

It has long been proposed that TRPC channels underlie the store-operated channels (SOC) observed in many cell types. These channels open due to the depletion of intracellular calcium stores. Two other proteins, stromal interaction molecules (STIMs) and the ORAIs, however, have more recently been implicated in this process. STIM1 and TRPC1 can coassemble, complicating the understanding of this phenomenon.

TRPC6 has been implicated in late onset Alzheimer's disease.

Research on the role of TRPC channels in cardiomyopathies is still in progress. An upregulation of TRPC1, TRPC3, and TRPC6 genes are seen in heart disease states including fibroblast formation and cardiovascular disease. The TRPC channels are suspected of responding to an overload of hormonal and mechanical stimulation in cardiovascular disease, contributing to pathological remodelling of the heart.

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