TRPC4
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Transient receptor potential cation channel, subfamily C, member 4, also known as TRPC4, is a human gene encoding a protein of the same name.
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[edit] Interactions
TRPC4 has been shown to interact with TRPC1,[1][2] ITPR1[3][4] and TRPC5.[2]
[edit] Roles
A 2011 study showed that deletion of the trpc4 gene in rats decreased levels of sociability in a social exploration task. These results suggest that TRPC4 may play a role in regulating social anxiety in a number of different disorders[5] . However, a 2012 study showed that deletion of the trpc4 gene had no impact on basic or strategic learning.[6]
[edit] Expression
The nonselective cation channel TRPC4 has been shown to be present in high abundance in the corticolimbic regions of the brain. A 2011 study found that TRPC4 mRNA is present in the VTA and the substantia nigra. [7]
[edit] See also
[edit] Further reading
- Islam, Md. Shahidul (January 2011). Transient Receptor Potential Channels. Advances in Experimental Medicine and Biology. 704. Berlin: Springer. pp. 700. ISBN 978-94-007-0264-6.
- Clapham DE, Julius D, Montell C, Schultz G (2006). "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.
- Cavalié A (2007). Ionic Channels Formed by TRPC4. "Ionic channels formed by TRPC4.". Handb Exp Pharmacol. Handbook of Experimental Pharmacology 179 (179): 93–108. doi:10.1007/978-3-540-34891-7_5. ISBN 978-3-540-34889-4. PMID 17217052.
[edit] References
- ^ Strübing, Carsten; Krapivinsky Grigory, Krapivinsky Luba, Clapham David E (Oct. 2003). "Formation of novel TRPC channels by complex subunit interactions in embryonic brain". J. Biol. Chem. (United States) 278 (40): 39014–9. doi:10.1074/jbc.M306705200. ISSN 0021-9258. PMID 12857742.
- ^ a b Hofmann, Thomas; Schaefer Michael, Schultz Günter, Gudermann Thomas (May. 2002). "Subunit composition of mammalian transient receptor potential channels in living cells". Proc. Natl. Acad. Sci. U.S.A. (United States) 99 (11): 7461–6. doi:10.1073/pnas.102596199. ISSN 0027-8424. PMC 124253. PMID 12032305. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=124253.
- ^ Yuan, Joseph P; Kiselyov Kirill, Shin Dong Ming, Chen Jin, Shcheynikov Nikolay, Kang Shin H, Dehoff Marlin H, Schwarz Martin K, Seeburg Peter H, Muallem Shmuel, Worley Paul F (Sep. 2003). "Homer binds TRPC family channels and is required for gating of TRPC1 by IP3 receptors". Cell (United States) 114 (6): 777–89. doi:10.1016/S0092-8674(03)00716-5. ISSN 0092-8674. PMID 14505576.
- ^ Mery, L; Magnino F, Schmidt K, Krause K H, Dufour J F (Jan. 2001). "Alternative splice variants of hTrp4 differentially interact with the C-terminal portion of the inositol 1,4,5-trisphosphate receptors". FEBS Lett. (Netherlands) 487 (3): 377–83. doi:10.1016/S0014-5793(00)02362-0. ISSN 0014-5793. PMID 11163362.
- ^ Rasmus, Kristin; Jun-Gang Wang, Andrew L. Varnell, Eric M. Ostertag, John P. Christianson & Donald C. Cooper (September 7). "Sociability is decreased following deletion of the trpc4 gene". Nature Precedings. doi:<http://dx.doi.org/10.1038/npre.2011.6367.1>. http://www.neuro-cloud.net/nature-precedings/rasmus.
- ^ Klipec, William D.; Phuong Nguyen, Bridget Deeney, Claire Williamson, Kami Wenzel, Jessica Stumme, Marissa Collins, Abby Drish, Laura Swenson, Eric Ostertag, Donald C. Cooper (24 February 2012). "Deletion of the trpc4 gene and its role in simple and complex strategic learning". Nature Precedings. doi:<http://dx.doi.org/10.1038/npre.2012.6929.1>. http://precedings.nature.com/documents/6929/version/1.
- ^ Illig, Kurt R.; Andrew L. Varnell, Eric M. Ostertag, William D. Klipec & Donald C. Cooper (11/7/11). "TRPC4 ion channel protein is selectively expressed in a subpopulation of dopamine neurons in the ventral tegmental area". Nature Precedings. doi:<http://dx.doi.org/10.1038/npre.2011.6577.1>. http://www.neuro-cloud.net/nature-precedings/illig.
[edit] External links
This article incorporates text from the United States National Library of Medicine, which is in the public domain.
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