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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. Structurally, this family shares 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.[1]

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. [2]

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.[1]

TRPC6 and TRPC4 have been implicated in late onset Alzheimer's disease.[3][4][5]



  1. ^ a b Nilius B, Owsianik G, Voets T, Peters JA (2007). "Transient receptor potential cation channels in disease". Physiol. Rev. 87 (1): 165–217. doi:10.1152/physrev.00021.2006. PMID 17237345.  
  2. ^ S. Z. Xu, P. Sukumar, F. Zeng et al. (2008). "TRPC channel activation by extracellular thioredoxin". Nature 7174: 69–72. doi:10.1038/nature06414. PMID 18172497.  
  3. ^ Lessard CB, Lussier MP, Cayouette S, Bourque G, Boulay G. (2005). "The overexpression of presenilin2 and Alzheimer's-disease-linked presenilin2 variants influences TRPC6-enhanced Ca2+ entry into HEK293 cells.". Cell Signal 17: 437–445. doi:10.1016/j.cellsig.2004.09.005.  
  4. ^ "Families shed light on likely causative gene for Alzheimer's".  
  5. ^ Poduslo SE, Huang R, Huang J, Smith S (2008-04-30 [Epub ahead of print]). "Genome screen of late-onset Alzheimer's extended pedigrees identifies TRPC4AP by haplotype analysis.". Am J Med Genet B Neuropsychiatr Genet 150b: 50. doi:10.1002/ajmg.b.30767. PMID 18449908.  

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