TRPM3: Difference between revisions
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'''Transient receptor potential cation channel subfamily M member 3''' is a [[protein]] that in humans is encoded by the ''TRPM3'' [[gene]].<ref name="pmid16382100">{{cite journal | vauthors = Clapham DE, Julius D, Montell C, Schultz G | title = International Union of Pharmacology. XLIX. Nomenclature and structure-function relationships of transient receptor potential channels | journal = | '''Transient receptor potential cation channel subfamily M member 3''' is a [[protein]] that in humans is encoded by the ''TRPM3'' [[gene]].<ref name="pmid16382100">{{cite journal | vauthors = Clapham DE, Julius D, Montell C, Schultz G | title = International Union of Pharmacology. XLIX. Nomenclature and structure-function relationships of transient receptor potential channels | journal = Pharmacological Reviews | volume = 57 | issue = 4 | pages = 427–50 | date = December 2005 | pmid = 16382100 | pmc = | doi = 10.1124/pr.57.4.6 }}</ref> | ||
== Function == | |||
==See also== | The product of this gene belongs to the family of [[transient receptor potential]] (TRP) channels. TRP channels are cation-selective [[ion channel|channels]] important for cellular [[calcium signaling]] and [[homeostasis]]. The protein encoded by this gene mediates calcium entry, and this entry is potentiated by calcium store depletion. Alternatively spliced transcript variants encoding different isoforms have been -identified.<ref>{{cite web | title = Entrez Gene: TRPM3 transient receptor potential cation channel, subfamily M, member 3| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=80036| access-date = }}</ref> | ||
TRPM3 was shown to be activated by the [[neurosteroid]] [[pregnenolone]] sulphate in pancreatic [[beta cell]]. The activation causes [[calcium]] influx and subsequent [[insulin release]], therefore it is suggested that TRPM3 modulates [[glucose]] homeostasis.<ref name="pmid18978782">{{cite journal | vauthors = Wagner TF, Loch S, Lambert S, Straub I, Mannebach S, Mathar I, Düfer M, Lis A, Flockerzi V, Philipp SE, Oberwinkler J | title = Transient receptor potential M3 channels are ionotropic steroid receptors in pancreatic beta cells | journal = Nature Cell Biology | volume = 10 | issue = 12 | pages = 1421–30 | date = December 2008 | pmid = 18978782 | doi = 10.1038/ncb1801 }}</ref> | |||
==TRPM3 Ligands== | |||
===Channel Blockers=== | |||
#[[Mefenamic acid]]<ref name="KloseStraub2011">{{cite journal | vauthors = Klose C, Straub I, Riehle M, Ranta F, Krautwurst D, Ullrich S, Meyerhof W, Harteneck C | title = Fenamates as TRP channel blockers: mefenamic acid selectively blocks TRPM3 | journal = British Journal of Pharmacology | volume = 162 | issue = 8 | pages = 1757–69 | date = April 2011 | pmid = 21198543 | doi = 10.1111/j.1476-5381.2010.01186.x }}</ref> | |||
#[[Citrus fruit]] [[flavonoids]], E.g. [[Naringenin]] and [[hesperetin]], as well as [[Ononetin]] (a [[deoxybenzoin]]).<ref name="StraubMohr2013">{{cite journal | vauthors = Straub I, Mohr F, Stab J, Konrad M, Philipp SE, Oberwinkler J, Schaefer M | title = Citrus fruit and fabacea secondary metabolites potently and selectively block TRPM3 | journal = British Journal of Pharmacology | volume = 168 | issue = 8 | pages = 1835–50 | date = April 2013 | pmid = 23190005 | doi = 10.1111/bph.12076 }}</ref> | |||
===Agonist=== | |||
*[[CIM0216]] | |||
== See also == | |||
* [[TRPM]] | * [[TRPM]] | ||
==References== | == References == | ||
{{reflist}} | {{reflist}} | ||
==Further reading== | == Further reading == | ||
{{refbegin | 2}} | {{refbegin | 2}} | ||
*{{cite journal | * {{cite journal | vauthors = Oberwinkler J, Phillipp SE | title = TRPM3 | journal = Handbook of Experimental Pharmacology | volume = 179 | issue = 179 | pages = 253–67 | year = 2007 | pmid = 17217062 | doi = 10.1007/978-3-540-34891-7_15 }} | ||
*{{cite journal | * {{cite journal | vauthors = Harteneck C, Reiter B | title = TRP channels activated by extracellular hypo-osmoticity in epithelia | journal = Biochemical Society Transactions | volume = 35 | issue = Pt 1 | pages = 91–5 | date = February 2007 | pmid = 17233610 | doi = 10.1042/BST0350091 }} | ||
* {{cite journal | vauthors = Held K, Voets T, Vriens J | title = TRPM3 in temperature sensing and beyond | journal = Temperature | volume = 2 | issue = 2 | pages = 201–13 | date = 2014 | pmid = 27227024 | pmc = 4844244 | doi = 10.4161/23328940.2014.988524 }} | |||
* {{cite book | editor-last=Islam | editor-first=Md. Shahidul | year=2011 | title = Transient Receptor Potential Channels | url = http://trpbook.islets.se | series = Advances in Experimental Medicine and Biology | volume = 704 | publication-place=New York | publisher=Springer Science+Business Media | doi = 10.1007/978-94-007-0265-3 | isbn = 978-94-007-0265-3 | issn = 2214-8019 | oclc=710148029 | ref=harv}} | |||
{{refend}} | {{refend}} | ||
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[[Category:Ion channels]] | [[Category:Ion channels]] | ||
{{membrane-protein-stub}} | {{membrane-protein-stub}} | ||
Latest revision as of 07:31, 10 January 2019
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Transient receptor potential cation channel subfamily M member 3 is a protein that in humans is encoded by the TRPM3 gene.[1]
Function
The product of this gene belongs to the family of transient receptor potential (TRP) channels. TRP channels are cation-selective channels important for cellular calcium signaling and homeostasis. The protein encoded by this gene mediates calcium entry, and this entry is potentiated by calcium store depletion. Alternatively spliced transcript variants encoding different isoforms have been -identified.[2] TRPM3 was shown to be activated by the neurosteroid pregnenolone sulphate in pancreatic beta cell. The activation causes calcium influx and subsequent insulin release, therefore it is suggested that TRPM3 modulates glucose homeostasis.[3]
TRPM3 Ligands
Channel Blockers
- Mefenamic acid[4]
- Citrus fruit flavonoids, E.g. Naringenin and hesperetin, as well as Ononetin (a deoxybenzoin).[5]
Agonist
See also
References
- ↑ 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". Pharmacological Reviews. 57 (4): 427–50. doi:10.1124/pr.57.4.6. PMID 16382100.
- ↑ "Entrez Gene: TRPM3 transient receptor potential cation channel, subfamily M, member 3".
- ↑ Wagner TF, Loch S, Lambert S, Straub I, Mannebach S, Mathar I, Düfer M, Lis A, Flockerzi V, Philipp SE, Oberwinkler J (December 2008). "Transient receptor potential M3 channels are ionotropic steroid receptors in pancreatic beta cells". Nature Cell Biology. 10 (12): 1421–30. doi:10.1038/ncb1801. PMID 18978782.
- ↑ Klose C, Straub I, Riehle M, Ranta F, Krautwurst D, Ullrich S, Meyerhof W, Harteneck C (April 2011). "Fenamates as TRP channel blockers: mefenamic acid selectively blocks TRPM3". British Journal of Pharmacology. 162 (8): 1757–69. doi:10.1111/j.1476-5381.2010.01186.x. PMID 21198543.
- ↑ Straub I, Mohr F, Stab J, Konrad M, Philipp SE, Oberwinkler J, Schaefer M (April 2013). "Citrus fruit and fabacea secondary metabolites potently and selectively block TRPM3". British Journal of Pharmacology. 168 (8): 1835–50. doi:10.1111/bph.12076. PMID 23190005.
Further reading
- Oberwinkler J, Phillipp SE (2007). "TRPM3". Handbook of Experimental Pharmacology. 179 (179): 253–67. doi:10.1007/978-3-540-34891-7_15. PMID 17217062.
- Harteneck C, Reiter B (February 2007). "TRP channels activated by extracellular hypo-osmoticity in epithelia". Biochemical Society Transactions. 35 (Pt 1): 91–5. doi:10.1042/BST0350091. PMID 17233610.
- Held K, Voets T, Vriens J (2014). "TRPM3 in temperature sensing and beyond". Temperature. 2 (2): 201–13. doi:10.4161/23328940.2014.988524. PMC 4844244. PMID 27227024.
- Islam, Md. Shahidul, ed. (2011). Transient Receptor Potential Channels. Advances in Experimental Medicine and Biology. 704. New York: Springer Science+Business Media. doi:10.1007/978-94-007-0265-3. ISBN 978-94-007-0265-3. ISSN 2214-8019. OCLC 710148029.
External links
- TRPM3+protein,+human at the US National Library of Medicine Medical Subject Headings (MeSH)
This article incorporates text from the United States National Library of Medicine, which is in the public domain.
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