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quantitative FRET analysis in acutely isolated cone OS revealed that the cone degeneration-causing V268I mutation in peripherin-2 (zeige PRPH2 Proteine) selectively reduced binding to M-opsin without affecting the peripherin-2 (zeige PRPH2 Proteine) interaction to S-opsin (zeige OPN1SW Proteine) or rhodopsin (zeige RHO Proteine)
Luciferase expression driven by the midwavelength sensitive opsin intron 3-4 region was only slightly increased by THRB2 (zeige THRB Proteine), and rather enhanced by COUP-TFII (zeige NR2F2 Proteine).
ectopically expressed cTalpha (zeige PCYT1A Proteine) 1) forms a heterotrimeric complex with rod Gbeta (zeige SUCLG2 Proteine)(1)gamma(1), and substitutes equally for rTalpha in generating photoresponses initiated by either rhodopsin (zeige RHO Proteine) or S-cone opsin (zeige RHO Proteine)
results show that UV-opsin (zeige RHO Proteine) suppression successively ceases in presence of the M-opsin activating background light, which implies that cone light adaptation is controlled at the opsin (zeige RHO Proteine) stage, before activation of transducin (zeige GNAT1 Proteine).
Thus, the three types of mouse opsin (zeige RHO Proteine) appear distinctive in the degree to which their bleached, unregenerated opsins generate "dark light."
alpha transducin (zeige GNAT1 Proteine) and opsin (zeige RHO Proteine) have roles in mouse photoreceptor cell responses to light and dark
OPN1LW and OPN1MW restore M-cone function in a mouse model of human blue cone monochromacy.
By inserting five different thermostabilizing proteins (BRIL (zeige IFITM5 Proteine), T4L, PGS, RUB (zeige RXRB Proteine), 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 (zeige RHO Proteine) mutations.
Missense mutatin in both OPN1LW and OPN1MW cause X-linked cone dystrophy.
Mutations in the LW/MW cone opsin (zeige RHO Proteine) gene array can, therefore, lead to a spectrum of disease, ranging from color blindness to progressive cone dystrophy (XLCOD5).
The apparent decline in opsin (zeige RHO Proteine) 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
, green opsin
, opsin 1 (cone pigments), medium-wave-sensitive
, green-sensitive opsin-like