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TRPM1 encodes a member of the transient receptor potential melastatin subfamily of transient receptor potential ion channels. Additionally we are shipping TRPM1 Antibodies (14) and TRPM1 Kits (3) and many more products for this protein.
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Evidence for a retroviral insertion in TRPM1 as the cause of congenital stationary night blindness and leopard complex spotting in the horse.
In the Miniature Horse, congenital stationary night blindness is perfectly associated with leopard complex spotting patterns and SNPs in the candidate gene TRPM1.
Re-sequencing of the gene and associated splice sites within the 105 624 bp genomic region of TRPM1 led to the discovery of 18 SNPs.
Decreased expression of TRPM1 in the eye and the skin may alter bipolar cell signaling as well as melanocyte function, thus causing both stationary night blindness and coat spotting patterns in horses.
genotype-phenotype correlations showed that this eye phenotype was secondary to homozygous deletion of TRPM1, the gene responsible for autosomal recessive congenital stationary night blindness. The main differential diagnosis is ceroid lipofuscinosis.
these data indicate that purified TRPM1 is mostly dimeric. The three-dimensional structure of TRPM1 dimers is characterized by a small putative transmembrane domain and a larger domain with a hollow cavity.
visual deficits in melanoma associated (show ZNF654 Proteins) retinopathy are caused by the uptake of TRPM1 autoantibodies into ON-bipolar cells
This is the first reported case of a melanoma-associated (show ZNF654 Proteins) retinopathy diagnosed utilizing the innovative approach of testing for serum TRPM1 autoantibodies.
These data suggest differences in coupling of TRPM1 function to mGluR6 (show GRM6 Proteins) signaling explain different cellular responses to glutamate (show GRIN1 Proteins) in the retina and the skin.
We found 13 different mutations in the TRPM1 gene in congenital stationary night blindness.
The results expand the mutation spectrum of NYX (show NYX Proteins), CACNA1F (show CACNA1F Proteins) and GRM6 (show GRM6 Proteins). They also suggest that NYX (show NYX Proteins) mutations are a common cause of congenital stationary night blindness (CSNB (show CSN2 Proteins)),No variations were found in TRPM1.
present investigation found no evidence for an association between sequence variation at the TRPM1 gene and albumin (show ALB Proteins)-to-creatinine ratio in Mexican Americans, although it appears to have modest influence on T2DM risk factors
In the human retina TRPM1 is expressed on ON-bipolar cell dendrites that invaginate photoreceptor terminals and is also expressed on the synaptic ribbons of a subclass of rods, suggesting a dual function for TRPM1 in the ON-pathway.
A proteomic search for proteins associated with nyctalopin (show NYX Proteins) in the retina identifies TRPM1 as the binding partner.
This study confirmed the localization of LRIT3 at the dendritic tips of depolarizing bipolar cells in mouse retina and demonstrated the dependence of TRPM1 localization on the presence of LRIT3.
results indicate that the serum of a patient with PR contained an antibody against TRPM1 caused an acute death of retinal ON bipolar cells of mice
TRPM1 is not essential for the development of hearing or balance in the mouse model and it is unlikely that TRPM1 is the hair cell mechanotransduction channel.
The data indicates that the A1068T mutant TRPM1 acts as a dominant negative with respect to TRPM1 channel function.
Results suggest a model in which the Gbetagamma dimer that is released as a result of the dissociation from Galpha(o (show GNAO1 Proteins)) upon activation of mGluR6 (show GRM6 Proteins) closes the TRPM1 channel, perhaps via a direct interaction.
The results suggested that the TRPM1 channel in metabotropic glutamate receptor 6 (show GRM6 Proteins)-null rod bipolar cells is inactive. Rod bipolar cells in metabotropic glutamate receptor 6 (show GRM6 Proteins)-null mice were hyperpolarized.
TRPM1 is involved in non-image-forming responses to light and may perform a functional role within photosensitive retinal ganglion cells
This review describes the differential expression of TRPM1-S (short form) and -L (long form) in the mouse retina. TRPM1-L encodes a predicted 1,622 amino acid protein containing six transmembrane domains.
Human TRPM1 mutations are associated with the complete form of congenital stationary night blindness in Japanese patients.
These results demonstrate that TRPM1-L is a component of the ON bipolar cell (BC) transduction channel downstream of mGluR6 in ON BCs.
This gene encodes a member of the transient receptor potential melastatin subfamily of transient receptor potential ion channels. The encoded protein is a calcium permeable cation channel that is expressed in melanocytes and may play a role in melanin synthesis. Specific mutations in this gene are the cause autosomal recessive complete congenital stationary night blindness-1C. The expression of this protein is inversely correlated with melanoma aggressiveness and as such it is used as a prognostic marker for melanoma metastasis. Alternate splicing results in multiple transcript variants.
transient receptor potential cation channel, subfamily M, member 1
, transient receptor potential melastatin 1b
, transient receptor potential cation channel subfamily M member 1-like
, long transient receptor potential channel 1
, transient receptor potential cation channel subfamily M member 1
, transient receptor potential melastatin family
, melastatin 1