TRPM8: Difference between revisions

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'''Transient receptor potential cation channel, subfamily M, member 8''', also known as '''TRPM8''', is a human [[gene]]. The TRPM8 protein is expresed in sensory neurons, and it is activated by cold temperatures and cooling agents, such as [[menthol]] and [[icilin]] where as CPS-369 is the most selective agonist of TRPM8<ref>Sherkheli MA, et al., (2007) Selective TRPM8 agonists: a novel group of neuropathic analgesics. [[FEBS Journal]], 274(S1). 232–232.</ref>. TRPM8 is an ion channel, upon activation it allows the entry of Na<sup>+</sup> ([[sodium]]) and Ca<sup>2+</sup> ([[calcium]]) ions to the cell that leads to depolarization and the generation of action potential. This eventually leads to the feeling of cold. Cold-patches have traditionally been used to induce [[analgesia]] or relief in pain which is caused as result of traumatic injuries. The underlying mechanism of cold-induced [[analgesia]] remained obscure till the discovery of TRPM8. Three independent research groups have reported that mice lacking TRPM8 gene are severely impaired in their ability to detect [[cold]] temperatures<ref>Daniels RL, et al., (2007) Mice left out in the cold: commentary on the phenotype of TRPM8-nulls. [[Molecular Pain]], 3: 23.</ref>. Remarkably, these animals are deficient in many diverse aspects of [[cold signaling]], including cool and [[noxious cold perception]], injury-evoked sensitization to cold, and [[cooling-induced analgesia]]. These animals provide a great deal of insight into the molecular signaling pathways that participate in the detection of cold and painful stimuli. Many groups are now actively involved in looking for selective TRPM8 [[ligands]] to be used as new generation of [[neuropathic]] analgesic drugs.
'''Transient receptor potential cation channel, subfamily M, member 8''', also known as '''TRPM8''', is a human [[gene]]. The TRPM8 protein is expresed in sensory neurons, and it is activated by cold temperatures and cooling agents, such as [[menthol]] and [[icilin]] where as CPS-369 is the most selective agonist of TRPM8.<ref>{{cite journal |author=Sherkeli et al. |title=Selective TRPM8 agonists: a novel group of neurophathic analgesics |journal=FEBS Journal |volume=274 |issue=s1 |pages=232 |year=2007 |month= |pmid= |doi=10.1111/j.0014-2956.2007.05861_4.x |url=}}<ref> TRPM8 is an ion channel, upon activation it allows the entry of Na<sup>+</sup> ([[sodium]]) and Ca<sup>2+</sup> ([[calcium]]) ions to the cell that leads to depolarization and the generation of action potential. This eventually leads to the feeling of cold. Cold-patches have traditionally been used to induce [[analgesia]] or relief in pain which is caused as result of traumatic injuries. The underlying mechanism of cold-induced [[analgesia]] remained obscure till the discovery of TRPM8. Three independent research groups have reported that mice lacking TRPM8 gene are severely impaired in their ability to detect [[cold]] temperatures.<ref name="pmid17705869">{{cite journal |author=Daniels RL, McKemy DD |title=Mice left out in the cold: commentary on the phenotype of TRPM8-nulls |journal=Mol Pain |volume=3 |issue= |pages=23 |year=2007 |pmid=17705869 |pmc=1988789 |doi=10.1186/1744-8069-3-23 |url=}}</ref> Remarkably, these animals are deficient in many diverse aspects of [[cold signaling]], including cool and [[noxious cold perception]], injury-evoked sensitization to cold, and [[cooling-induced analgesia]]. These animals provide a great deal of insight into the molecular signaling pathways that participate in the detection of cold and painful stimuli. Many research groups, both in universities and pharmaceutical companies, are now actively involved in looking for selective TRPM8 [[ligands]] to be used as new generation of [[neuropathic]] analgesic drugs.



Revision as of 20:11, 11 June 2008

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TRPM8
Identifiers
AliasesTRPM8, LTRPC6, TRPP8, transient receptor potential cation channel subfamily M member 8, trp-p8, LTrpC-6
External IDsOMIM: 606678; MGI: 2181435; HomoloGene: 23433; GeneCards: TRPM8; OMA:TRPM8 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_024080

NM_134252

RefSeq (protein)

NP_076985

NP_599013

Location (UCSC)Chr 2: 233.92 – 234.02 MbChr 1: 88.21 – 88.32 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Transient receptor potential cation channel, subfamily M, member 8, also known as TRPM8, is a human gene. The TRPM8 protein is expresed in sensory neurons, and it is activated by cold temperatures and cooling agents, such as menthol and icilin where as CPS-369 is the most selective agonist of TRPM8.Cite error: A <ref> tag is missing the closing </ref> (see the help page). Remarkably, these animals are deficient in many diverse aspects of cold signaling, including cool and noxious cold perception, injury-evoked sensitization to cold, and cooling-induced analgesia. These animals provide a great deal of insight into the molecular signaling pathways that participate in the detection of cold and painful stimuli. Many research groups, both in universities and pharmaceutical companies, are now actively involved in looking for selective TRPM8 ligands to be used as new generation of neuropathic analgesic drugs.


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See also

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000144481Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000036251Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.

Further reading

External links

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