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quantitative FRET analysis in acutely isolated cone OS revealed that the cone degeneration-causing V268I mutation in peripherin-2 (Montrer PRPH2 Protéines) selectively reduced binding to M-opsin without affecting the peripherin-2 (Montrer PRPH2 Protéines) interaction to S-opsin (Montrer OPN1SW Protéines) or rhodopsin (Montrer RHO Protéines)
Luciferase expression driven by the midwavelength sensitive opsin intron 3-4 region was only slightly increased by THRB2 (Montrer THRB Protéines), and rather enhanced by COUP-TFII (Montrer NR2F2 Protéines).
ectopically expressed cTalpha (Montrer PCYT1A Protéines) 1) forms a heterotrimeric complex with rod Gbeta (Montrer SUCLG2 Protéines)(1)gamma(1), and substitutes equally for rTalpha in generating photoresponses initiated by either rhodopsin (Montrer RHO Protéines) or S-cone opsin (Montrer RHO Protéines)
results show that UV-opsin (Montrer RHO Protéines) suppression successively ceases in presence of the M-opsin activating background light, which implies that cone light adaptation is controlled at the opsin (Montrer RHO Protéines) stage, before activation of transducin (Montrer GNAT1 Protéines).
Thus, the three types of mouse opsin (Montrer RHO Protéines) appear distinctive in the degree to which their bleached, unregenerated opsins generate "dark light."
alpha transducin (Montrer GNAT1 Protéines) and opsin (Montrer RHO Protéines) have roles in mouse photoreceptor cell responses to light and dark
By inserting five different thermostabilizing proteins (BRIL (Montrer IFITM5 Protéines), T4L, PGS, RUB (Montrer RXRB Protéines), and FLAV) into the recombinant green opsin sequence, constructs were created that were up to 9-fold more stable than WT.
Investigated 24 affected males with blue cone monochromacy from 16 families with either a structurally intact gene cluster or at least one intact single (hybrid) gene but harbouring rare combinations of common SNPs in exon 3 in single or multiple OPN1LW and OPN1MW gene copies. We could establish intrachromosomal gene conversion in the male germline as underlying mechanism.
Findings show that mutation in OPN1MW underlie the cone dysfunction in all of the subjects tested, the color vision defect can be caused either by the same mutation or a gene rearrangement at the same locus.
Data suggest that OPN1MW exhibits a conserved Pro-Pro motif in extracellular loop 2 as observed in monostable visual G-protein-coupled receptors; comparison of deuterium uptake between inactive and active states of OPN1MW suggests a reduced solvent accessibility of the extracellular N-terminal region and an increased accessibility of the chromophore binding site.
Data suggest that insights into dimerization interface of red cone opsin should aid investigations of the structure and function of GPCR cell signaling.
Identification of one single red-green OPN1LW/MW hybrid gene harboring a point mutation that associates with blue cone monochromatism.
The photoreceptor phenotype associated with OPN1LW and OPN1MW mutations is highly variable. These findings have implications for the potential restoration of visual function in subjects with opsin (Montrer RHO Protéines) mutations.
Missense mutatin in both OPN1LW and OPN1MW cause X-linked cone dystrophy.
Mutations in the LW/MW cone opsin (Montrer RHO Protéines) gene array can, therefore, lead to a spectrum of disease, ranging from color blindness to progressive cone dystrophy (XLCOD5).
In Japanese males with congenital red/green color blindness the mutation Asn94Lys (AAC-->AAA) occurred in the single green gene of a deutan subject (A155); and Arg330Gln (CGA-->CAA) in both green genes of another, affecting protein folding and function
The apparent decline in opsin (Montrer RHO Protéines) 1 opponency from superior to inferior retina is consistent with the dual gradient and a model where photoreceptor signals in both superior and inferior retina
This gene encodes for a light absorbing visual pigment of the opsin gene family. The encoded protein is called green cone photopigment or medium-wavelength sensitive opsin. Opsins are G-protein coupled receptors with seven transmembrane domains, an N-terminal extracellular domain, and a C-terminal cytoplasmic domain. The long-wavelength opsin gene and multiple copies of the medium-wavelength opsin gene are tandemly arrayed on the X chromosome and frequent unequal recombination and gene conversion may occur between these sequences. X chromosomes may have fusions of the medium- and long-wavelength opsin genes or may have more than one copy of these genes. Defects in this gene are the cause of deutanopic colorblindness.
, green LWS photopigment
, green cone photoreceptor pigment
, green long wavelength sensitive cone opsin
, green-sensitive opsin
, medium wavelength-sensitive cone opsin
, medium-wave-sensitive opsin 1
, midwavelength sensitive opsin
, green sensitive cone opsin
, opsin CHK-1
, cone dystrophy 5 (X-linked)
, green cone pigment
, photopigment apoprotein
, opsin 1 (cone pigments), medium-wave-sensitive (color blindness, deutan), green opsin
, long-wave-sensitive opsin 1
, opsin 1 (cone pigments), long-wave-sensitive (color blindness, protan)
, opsin 1 (cone pigments), medium-wave-sensitive (color blindness, deutan)
, opsin 1 (cone pigments), medium-wave-sensitive 2
, red cone photoreceptor pigment
, red opsin
, red-sensitive opsin
, opsin 1, long-wave-sensitive
, green opsin
, opsin 1 (cone pigments), medium-wave-sensitive
, green-sensitive opsin-like