Transient receptor potential cation channel subfamily M member 1 is a
protein that in humans is encoded by the TRPM1gene.[5][6][7]
Function
The protein encoded by this gene is a member of the
transient receptor potential (TRP) family of non-selective cation
channels. It is expressed in the retina, in a subset of
bipolar cells termed ON bipolar cells.[8][9] These cells form
synapses with either
rods or
cones, collecting signals from them. In the dark, the signal arrives in the form of the
neurotransmitter glutamate, which is detected by a
G protein-coupled receptor (GPCR) signal transduction cascade. Detection of glutamate by the GPCR
Metabotropic glutamate receptor 6 results in closing of the TRPM1 channel. At the onset of light, glutamate release is halted and mGluR6 is deactivated; this results in opening of the TRPM1 channel, influx of sodium and calcium, and
depolarization of the bipolar cell.[10][11]
In addition to the retina, TRPM1 is also expressed in
melanocytes, which are melanin-producing cells in the skin. The expression of TRPM1 is inversely correlated with
melanoma aggressiveness, suggesting that it might suppress
melanomametastasis.[12] However, subsequent work showed that a
microRNA located in an
intron of the TRPM1 gene, rather than the TRPM1 protein itself, is responsible for the tumor suppressor function.[13][14] The expression of both TRPM1 and the microRNA are regulated by the
Microphthalmia-associated transcription factor.[15][16][17][13]
^"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^Hunter JJ, Shao J, Smutko JS, Dussault BJ, Nagle DL, Woolf EA, Holmgren LM, Moore KJ, Shyjan AW (Nov 1998). "Chromosomal localization and genomic characterization of the mouse melastatin gene (Mlsn1)". Genomics. 54 (1): 116–23.
doi:
10.1006/geno.1998.5549.
PMID9806836.
^Duncan LM, Deeds J, Hunter J, Shao J, Holmgren LM, Woolf EA, Tepper RI, Shyjan AW (Apr 1998). "Down-regulation of the novel gene melastatin correlates with potential for melanoma metastasis". Cancer Research. 58 (7): 1515–20.
PMID9537257.
^Clapham DE, Julius D, Montell C, Schultz G (Dec 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.
PMID16382100.
S2CID17936350.
Transient receptor potential cation channel subfamily M member 1 is a
protein that in humans is encoded by the TRPM1gene.[5][6][7]
Function
The protein encoded by this gene is a member of the
transient receptor potential (TRP) family of non-selective cation
channels. It is expressed in the retina, in a subset of
bipolar cells termed ON bipolar cells.[8][9] These cells form
synapses with either
rods or
cones, collecting signals from them. In the dark, the signal arrives in the form of the
neurotransmitter glutamate, which is detected by a
G protein-coupled receptor (GPCR) signal transduction cascade. Detection of glutamate by the GPCR
Metabotropic glutamate receptor 6 results in closing of the TRPM1 channel. At the onset of light, glutamate release is halted and mGluR6 is deactivated; this results in opening of the TRPM1 channel, influx of sodium and calcium, and
depolarization of the bipolar cell.[10][11]
In addition to the retina, TRPM1 is also expressed in
melanocytes, which are melanin-producing cells in the skin. The expression of TRPM1 is inversely correlated with
melanoma aggressiveness, suggesting that it might suppress
melanomametastasis.[12] However, subsequent work showed that a
microRNA located in an
intron of the TRPM1 gene, rather than the TRPM1 protein itself, is responsible for the tumor suppressor function.[13][14] The expression of both TRPM1 and the microRNA are regulated by the
Microphthalmia-associated transcription factor.[15][16][17][13]
^"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^Hunter JJ, Shao J, Smutko JS, Dussault BJ, Nagle DL, Woolf EA, Holmgren LM, Moore KJ, Shyjan AW (Nov 1998). "Chromosomal localization and genomic characterization of the mouse melastatin gene (Mlsn1)". Genomics. 54 (1): 116–23.
doi:
10.1006/geno.1998.5549.
PMID9806836.
^Duncan LM, Deeds J, Hunter J, Shao J, Holmgren LM, Woolf EA, Tepper RI, Shyjan AW (Apr 1998). "Down-regulation of the novel gene melastatin correlates with potential for melanoma metastasis". Cancer Research. 58 (7): 1515–20.
PMID9537257.
^Clapham DE, Julius D, Montell C, Schultz G (Dec 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.
PMID16382100.
S2CID17936350.