TRPC5

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Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

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RefSeq (protein)

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Short transient receptor potential channel 5 (TrpC5) also known as transient receptor protein 5 (TRP-5) is a protein that in humans is encoded by the TRPC5 gene.[1][2][3] TrpC5 is subtype of the TRPC family of mammalian transient receptor potential ion channels.

Function

TrpC5 is one of the seven mammalian TRPC (transient receptor potential canonical) proteins. TrpC5 is a multi-pass membrane protein and is thought to form a receptor-activated non-selective calcium permeant cation channel. The protein is active alone or as a heteromultimeric assembly with TRPC1, TRPC3, and TRPC4. It also interacts with multiple proteins including calmodulin, CABP1, enkurin, Na+–H+ exchange regulatory factor (NHERF), interferon-induced GTP-binding protein (MX1), ring finger protein 24 (RNF24), and SEC14 domain and spectrin repeat-containing protein 1 (SESTD1).[1]

TRPC4 and TRPC5 have been implicated in the mechanism of mercury toxicity[4] and neurological behavior.[5]

Activation

Homomultimeric TRPC5 and heteromultimeric TRPC5-TRPC1 channels are activated by extracellular reduced thioredoxin.[6] This channel has also been found to be involved in the action of anaesthetics such as chloroform, halothane and propofol.[7]

Interactions

TRPC5 has been shown to interact with STMN3,[8] TRPC1,[9][10] and TRPC4.[10]

See also

References

  1. 1.0 1.1 "Entrez Gene: transient receptor potential cation channel".
  2. Sossey-Alaoui K, Lyon JA, Jones L, Abidi FE, Hartung AJ, Hane B, Schwartz CE, Stevenson RE, Srivastava AK (September 1999). "Molecular cloning and characterization of TRPC5 (HTRP5), the human homologue of a mouse brain receptor-activated capacitative Ca2+ entry channel". Genomics. 60 (3): 330–40. doi:10.1006/geno.1999.5924. PMID 10493832.
  3. Clapham DE, Julius D, Montell C, Schultz G (December 2005). "International Union of Pharmacology. XLIX. Nomenclature and structure-function relationships of transient receptor potential channels". Pharmacol. Rev. 57 (4): 427–50. doi:10.1124/pr.57.4.6. PMID 16382100.
  4. Xu SZ, Zeng B, Daskoulidou N, Chen GL, Atkin SL, Lukhele B (January 2012). "Activation of TRPC cationic channels by mercurial compounds confers the cytotoxicity of mercury exposure". Toxicol. Sci. 125 (1): 56–68. doi:10.1093/toxsci/kfr268. PMID 21984481.
  5. Riccio A, Li Y, Moon J, Kim KS, Smith KS, Rudolph U, Gapon S, Yao GL, Tsvetkov E, Rodig SJ, Van't Veer A, Meloni EG, Carlezon WA, Bolshakov VY, Clapham DE (May 15, 2009). "Essential role for TRPC5 in amygdala function and fear-related behavior". Cell. 137 (4): 761–72. doi:10.1016/j.cell.2009.03.039. PMC 2719954. PMID 19450521.
  6. Xu SZ, Sukumar P, Zeng F, Li J, Jairaman A, English A, Naylor J, Ciurtin C, Majeed Y, Milligan CJ, Bahnasi YM, Al-Shawaf E, Porter KE, Jiang LH, Emery P, Sivaprasadarao A, Beech DJ (January 2008). "TRPC channel activation by extracellular thioredoxin". Nature. 451 (7174): 69–72. doi:10.1038/nature06414. PMC 2645077. PMID 18172497.
  7. Bahnasi YM, Wright HM, Milligan CJ, Dedman AM, Zeng F, Hopkins PM, Bateson AN, Beech DJ (April 2008). "Modulation of TRPC5 cation channels by halothane, chloroform and propofol". Br. J. Pharmacol. 153 (7): 1505–12. doi:10.1038/sj.bjp.0707689. PMC 2437913. PMID 18204473.
  8. Greka A, Navarro B, Oancea E, Duggan A, Clapham DE (August 2003). "TRPC5 is a regulator of hippocampal neurite length and growth cone morphology". Nat. Neurosci. 6 (8): 837–45. doi:10.1038/nn1092. PMID 12858178.
  9. Strübing C, Krapivinsky G, Krapivinsky L, Clapham DE (October 2003). "Formation of novel TRPC channels by complex subunit interactions in embryonic brain". J. Biol. Chem. 278 (40): 39014–9. doi:10.1074/jbc.M306705200. PMID 12857742.
  10. 10.0 10.1 Hofmann T, Schaefer M, Schultz G, Gudermann T (May 2002). "Subunit composition of mammalian transient receptor potential channels in living cells". Proc. Natl. Acad. Sci. U.S.A. 99 (11): 7461–6. doi:10.1073/pnas.102596199. PMC 124253. PMID 12032305.

Further reading

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.