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1 ificant effect on the activity of human blue cone opsin.
2 in rods, followed about 1 week later by M&L cone opsin.
3 e opsin and suppressing short-wavelength (S) cone opsin.
4 sin than like a classical vertebrate rod-and-cone opsin.
5 ctive cone pigment and constitutively active cone opsin.
6 eceptors expressing recoverin, rhodopsin, or cone opsin.
7 ons labeled with biotinylated PNA and anti-S cone opsin.
8 essed L/M cone opsin, and some coexpressed S cone opsin.
9 are positive for TULP1, recoverin, and blue cone opsin.
10 ULP1-reactive and some are positive for blue cone opsin.
11 or TULP1 and many are reactive for red/green cone opsin.
12 antiserum to short (S) -wavelength specific cone opsin.
13 psin, human green cone opsin, and human blue cone opsin.
14 e more similar for blue cone opsin and green cone opsin.
15 re suppressed expression of short wavelength cone opsin.
16 tor-specific genes such as rhodopsin and red cone opsin.
17 presumably because of the mistrafficking of cone opsins.
18 dium-wavelength (M) and short-wavelength (S) cone opsins.
19 te signal termination by phosphorylating the cone opsins.
20 f 11-cis-retinal, the chromophore of rod and cone opsins.
21 ion, are essentially invariant in rod versus cone opsins.
22 g of mCAR to light-activated, phosphorylated cone opsins.
23 fic genes in vivo, such as rhodopsin and the cone opsins.
24 e lambdamax of phylogenetically distant Sws2 cone opsins.
25 he chromophore residing in rhodopsin and the cone opsins.
26 f the batho-shifted intermediates of rod and cone opsins.
27 studied with photoactivated Rho but not with cone opsins.
28 sitive (S) and long wavelength-sensitive (L) cone opsins.
29 -translational modification of red and green cone opsins.
30 istently co-localizes with S- and M-types of cone opsins.
31 al organization and transcription of rod and cone opsins.
32 d normal subcellular compartmentalization of cone opsins.
33 cycle that supplies 11- cis-retinaldehyde to cone opsins.
35 ery similar G protein receptors, the rod and cone opsins, activates one and deactivates the other, co
36 that differ in color (i.e., ratio of L- to S-cone opsin activation) while providing identical melanop
40 ra to long/medium (L/M) -wavelength specific cone opsin and cone-specific alpha-transducin detected a
41 e hypothesis is proposed that it arises from cone opsin and disk membrane swelling triggered by isome
42 S) or long/medium (L/M) wavelength-sensitive cone opsin and either a structural protein (peripherin)
45 tinin, and then used antibodies against blue cone opsin and red-green cone opsin to identify the indi
48 in mice by activating medium-wavelength (M) cone opsin and suppressing short-wavelength (S) cone ops
49 nts identified the primary component as a UV cone opsin and the two minor components as the short wav
51 retinal thickness, and expression of rod and cone opsins and causes specific loss of photoreceptors.
52 ation of cone-specific genes, including both cone opsins and cone tranducin alpha subunit in Rpe65-/-
53 mistry was performed with antibodies against cone opsins and kinases GRK1 and GRK7 in postmortem norm
55 isingly, precedes both the expression of the cone opsins and the formation of synaptic contacts in th
56 responses initiated by either rhodopsin or S-cone opsin, and 3) exhibited similar light-activated tra
57 clic nucleotide-gated cation channel-3, blue-cone opsin, and beta-6-PDE) was evaluated by immunocytoc
58 cleotide-gated cation channel-3 [CNG3], blue-cone opsin, and cGMP phosphodiesterase [PDE]); were eval
59 photoreceptors expressing rod opsin and red cone opsin, and decreased the number of photoreceptors e
63 brillary acidic protein (GFAP), rhodopsin, S-cone opsin, and M/L-cone opsin were performed, as were a
65 ates were immunostained for calbindin or for cone opsins, and labeled cells and outer segments were c
66 -retinol with expressed human and salamander cone opsins, and to determine by microspectrophotometry
74 the first time in a mammalian species, that cone opsins are phosphorylated and that CAR binds to pho
77 e pigment that enables night vision, whereas cone opsins are the pigments responsible for color visio
79 the expression of melanopsin, rhodopsin and cone opsin, as well as other retinal markers (tyrosine h
80 ith the hypothesis that the dual gradient of cone opsins assists achromatic contrast detection agains
81 , the photochemical excitation of the violet cone opsin at 425 nm generates the batho intermediate at
87 ifferent from those of the classical rod and cone opsins but matching the standard profile of an opsi
89 ed significant decrease of cone-specific (MW cone opsin) but not rod-specific (rhodopsin) markers.
90 At the early stage of degeneration, rod and cone opsins, but not peripherin/RDS, exhibited prominent
91 lacking chromophore to exploit the fact that cone opsins, but not R-opsin, require chromophore for pr
92 , multi-site phosphorylation of both S and M cone opsins by in situ phosphorylation and isoelectric f
97 one cell survival was determined by counting cone opsin-containing cells on flat-mounted P30 retinas.
98 al modeling suggesting that Pro-205 in green cone opsin could prevent entry and binding of 11-cis-6mr
99 d by regeneration, were hybridized with blue cone opsin cRNA for quantitative analysis of the blue co
100 aining with antibodies to rod opsin, S and M cone opsins, cytochrome oxidase, synaptophysin, glial fi
101 otoreceptor-specific proteins, rhodopsin and cone opsins, decreased expression of the specific inflam
103 that either GRK7 or GRK1 may participate in cone opsin desensitization, depending on the expression
106 ngth appear to result from mistrafficking of cone opsins due to impaired delivery of retinaldehyde ch
107 cterized by functional loss of both L- and M-cone opsins due to mutations in the OPN1LW/OPN1MW gene c
109 tion, and apoptosis, plays a central role in cone opsin expression and patterning in the retina.
111 served that Pias3 directly regulated M and S cone opsin expression by modulating the cone-enriched tr
112 f pRGCs are spectrally tuned by gradients in cone opsin expression depending on their location in the
113 inhibitory surround receptive fields on the cone opsin expression gradient, and by introducing oppon
114 ofluorescence demonstrated the total loss of cone opsin expression in B. mysticetus, whereas light mi
115 suggests that separate enhancers control red cone opsin expression in DC-P and DC-A, consistent with
116 nvestigate the action of TH and RA on single-cone opsin expression in juvenile rainbow trout, zebrafi
117 tal expression of RXRgamma was examined, and cone opsin expression in RXRgamma-null mice was analyzed
118 e null mutation leads to altered topology of cone opsin expression in the retina, with aberrant S-ops
122 described the developmental pattern of human cone opsin expression, nor has the existence of human co
123 et-sensitive and medium-wavelength-sensitive cone opsin expression, produce dramatic variations in th
126 rod signals in retinal regions with sparse M-cone opsin expression.(10-13) The relative importance of
127 an be driven solely by cones, independent of cone-opsin expression gradients and rod input, with many
128 r degeneration with early mislocalization of cone opsins, features resembling those of Rpgr-null mice
131 nce of their natural ligand, 11-cis-retinal, cone opsin G-protein-coupled receptors fail to traffic n
132 cture of active-state, wild-type human green cone opsin (GCO(WT)) stabilized with a mini-G protein an
135 this would indicate that this rod-like green cone opsin gene, although absent in mammals, is common i
147 t rapid retinal release from an active-state cone opsin helps prevent signal saturation and enables r
148 and Asn(15), whereas human (h) red and green cone opsins (hOPSR and hOPSG, respectively) are N-glycos
151 at Rx is co-expressed with rhodopsin and red cone opsin in maturing photoreceptors and demonstrate th
156 otoreceptors exhibit ectopic localization of cone opsins in the cell body and synapses and rod photor
157 etermine whether the same effects on rod and cone opsins in the Rpe65-/- mouse are also present in th
158 The genes for the rod and rod-like green cone opsins in two avian species, the budgerigar, Melops
159 this deficit using mice expressing human red cone opsin, in which rod-, cone-, and melanopsin-depende
163 t lag between their expression and that of S cone opsin indicates that phototransduction proteins are
164 f the rate of thermal isomerization of mouse cone opsins, indicating that nonopsin sources of noise d
165 expression of the visual receptors, rod and cone opsins; inhibit the inflammatory reactions; and ind
166 ition, which governs the balance of S- and M-cone opsin input due to the opsin expression gradient in
170 hemically with cone-specific antibodies, and cone opsin levels were obtained by quantitative RT-PCR.
171 her cone photoreceptor cell number, improved cone opsin localization, and enhanced cone ERG signals w
173 mouse cone cells leads to mislocalization of cone opsin, loss of photopic electroretinogram (ERG) res
174 cone membrane-associated proteins including cone opsins (M- and S-opsins), cone transducin (Galphat2
175 vel and enzymatic activity of RPE65, causing cone opsin mislocalization and early cone degeneration i
176 ntly rods, accompanied by rhodopsin and blue cone opsin mislocalization from 6 to 12 months of age wi
177 intenance of photoreceptor function and that cone opsin mislocalization represents an early step in X
183 ongenital amaurosis and that the destructive cone opsin mistrafficking is caused by the lack of 11-ci
185 derived from long-wavelength sensitive (LWS) cone opsin mRNA identified several mutations in the opsi
192 ese results suggest that ventral and central cone opsins must be regenerated with 11-cis-retinal to p
193 e molecular mechanisms associated with these cone opsin mutants is fundamental to developing targeted
194 Studies on disease mechanisms due to these cone opsin mutations have been previously carried out ex
196 e find that the vertebrate medium wavelength cone opsin (MW-opsin) overcomes these limitations and su
198 served with bovine rhodopsin and human green cone opsin, on the picosecond to millisecond timescales
200 isms by which of rhodopsin (opsin 2) and the cone opsins (opsin 1) mediate vision, three other member
201 -long/medium wavelength-sensitive (anti-L/M) cone opsin or anti-glial fibrillary acidic protein (GFAP
202 mbined with labeling by either antibodies to cone opsins or biotinylated PNA, a consistent relationsh
203 retinas there was no evidence for any other cone opsins or pigments, rods, rod opsin expression, or
204 downregulation of the genes encoding rod and cone opsins, paralleled the decrease in ocular retinoid
205 letion of 16 N-terminal amino acids in green cone opsin partially restored the binding of 11-cis-6mr-
207 RXRgamma cooperates with TRbeta2 to regulate cone opsin patterning, the developmental expression of R
208 To elucidate the potential role of GRK1 in cone opsin phosphorylation, we created Nrl and Grk1 doub
209 Absorption of a photon by a rhodopsin or cone-opsin pigment isomerizes its 11-cis-retinaldehyde (
214 but further identification based on rod- or cone-opsin probes failed, suggesting the utilization of
215 ve transducin-stimulating activity, the free cone opsin produces an approximately 2-fold desensitizat
216 rAAV5-hCNGB3 with a long version of the red cone opsin promoter in younger animals led to a stable t
217 herapy with different forms of the human red cone opsin promoter led to the restoration of cone funct
221 photobleaching pathway of a short-wavelength cone opsin purified in delipidated form (lambda(max) = 4
222 aevis genes, Prph2 (also called RDS) and red cone opsin (RCO) using a polymerase chain reaction-based
223 which to investigate this issue, containing cone opsins red, green, blue, and violet, as well as the
228 udy highlights the much faster photocycle of cone opsins relative to Rho and the crucial role of RGR
229 rt because their activated state is unstable-cone opsins release their retinal agonist within seconds
231 old reductions in the mRNAs for M-cone and S-cone opsin, respectively, whereas there was no significa
232 mouse cone arrestin (mCAR) or mouse S and M cone opsins revealed specific binding of mCAR to light-a
233 n, medium-to-long wavelength-sensitive (M/L) cone opsin, rod opsin, excitatory amino acid transporter
234 , transgenically, short-wavelength-sensitive cone opsin (S-opsin) in rods and also lacking chromophor
235 c mice with rods expressing mouse short-wave cone opsin (S-opsin) to test whether cone pigment can su
240 of photoreceptors expressing the blue and UV cone opsins, suggesting targeted effects of RA on photor
241 fore they are reactive for blue or red/green cone opsin suggests an important role for TULP1 in devel
242 psins: one rod opsin, RH1 (498 nm), and five cone opsins, SWS1 (370 nm), SWS2B (408 nm), RH2B (498 nm
243 In contrast, a rod opsin (RH1) and three cone opsins (SWS2, RH2, and LWS) were expressed in postm
244 s suggest that the ligand is required during cone opsin synthesis for successful opsin trafficking an
245 comparable between bovine rhodopsin and blue cone opsin, the transition kinetics of earlier photo-int
246 ine loss of function mutations in rhodopsin, cone opsins, the V2 vasopressin receptor, ACTH receptor,
250 ammals such as mice use graded expression of cone opsins to extract visual information from their env
251 ects were associated with mislocalization of cone opsins to the nuclear and synaptic layers and reduc
252 nal before P25 led to increased transport of cone opsins to the outer segments and preserved cones an
255 e3 enhances rhodopsin, but represses S- or M-cone opsin transcription when interacting with Crx.
257 biochemically by expressing a Xenopus violet cone opsin (VCOP) cDNA in COS1 cells and assaying the li
258 3 in the Xenopus short-wavelength sensitive cone opsin (VCOP, lambda(max) approximately 427 nm).
261 ated controls, outer segment localization of cone opsin was improved, and ER stress/apoptotic cell de
262 that retinal hydrolysis from photoactivated cone opsins was markedly faster than from photoactivated
264 Our results suggest that subtle changes in L-cone opsin wavelength absorption may have been adaptive
269 ein (GFAP), rhodopsin, S-cone opsin, and M/L-cone opsin were performed, as were axon counts of the op
270 t P25, cone density and transcript levels of cone opsins were drastically reduced, but a minute cone
272 e to stimuli bleaching up to 99% of L- and M-cone opsins were measured with high resolution, phase-re
273 s, a substantial percentage of C150S-Rds and cone opsins were mislocalized to different cellular comp
275 he retina of these mice, the light-activated cone opsins were neither phosphorylated nor bound with m
276 imilar to C57BL/6 (wild-type) mice, and both cone opsins were properly localized to the cone outer se
277 rominent downregulation of middle wavelength cone opsin, whereas Rpe65(-)/(-) mice displayed more sup
278 on is a fundamental feature of red and green cone opsins, which may be relevant to their function or
279 termines the regeneration of mammalian green cone opsin with chromophore analogues such as 11-cis-6mr
280 the regenerative properties of rod and green cone opsins with 11-cis-6mr-retinal and demonstrated tha
281 By selectively stimulating the two mouse cone opsins with green and UV light, we assessed whether
282 n spectra conformed to the spectrum of green cone opsin, with a main sensitivity peak at 510 nm and a