TRPM2

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Transient receptor potential cation channel, subfamily M, member 2
Identifiers
Symbols TRPM2 ; EREG1; KNP3; LTRPC2; NUDT9H; NUDT9L1; TRPC7
External IDs OMIM603749 MGI1351901 HomoloGene20709 IUPHAR: 494 ChEMBL: 1250402 GeneCards: TRPM2 Gene
EC number 3.6.1.13
Orthologs
Species Human Mouse
Entrez 7226 28240
Ensembl ENSG00000142185 ENSMUSG00000009292
UniProt O94759 Q5KTC0
RefSeq (mRNA) NM_001001188 NM_138301
RefSeq (protein) NP_003298 NP_612174
Location (UCSC) Chr 21:
44.35 – 44.44 Mb
Chr 10:
77.91 – 77.97 Mb
PubMed search [1] [2]

Transient receptor potential cation channel, subfamily M, member 2, also known as TRPM2, is a protein that in humans is encoded by the TRPM2 gene.

Function

The TRPM2 gene is highly expressed in the brain and was implicated by both genetic linkage studies in families[1] and then by case control or trio allelic association studies in the genetic aetiology of bipolar affective disorder (Manic Depression).[2][3]

The physiological role of TRPM2 is not well understood. It was shown to be involved in insulin secretion.[4][5] In the immune cells it mediates parts of the responses to TNF-alpha.[6] A role has been suggested for TRPM2 in activation of NLRP3 inflammasome, the dysregulation of which is strongly associated with a number of auto inflammatory and metabolic diseases, such as gout, obesity and diabetes.[7] In the brain it is involved in the toxicity of amyloid beta, a protein associated with Alzheimer's disease.[8]

Structure

The protein encoded by this gene is a non-selective calcium-permeable cation channel and is part of the Transient Receptor Potential ion channel super family. The closest relative is the cold and menthol activated TRPM8 ion channel. While TRPM2 is not cold sensitive it is activated by heat.[4] The TRPM2 ion channel is activated by free intracellular ADP-ribose in synergy with free intracellular calcium.[9] ADP-Ribose is produced to by the enzyme PARP in response to oxidative stress and confers susceptibility to cell death. Several alternatively spliced transcript variants of this gene have been described, but their full-length nature is not known.[10]

See also

References

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Further reading

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External links

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

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