ライフサイエンスコーパス: 11-cis-retinal

1 ors of young mice lacking a normal supply of 11-cis retinal.

2 ear-wild-type levels and changed little with 11-cis retinal.

3 n the context of pharmacological rescue with 11-cis retinal.

4 s increased in Rpe65(-/-) cones on supplying 11-cis retinal.

5 imilarly, the Lrat-/- mouse does not produce 11-cis retinal.

6 levels were determined by regeneration with 11-cis retinal.

7 psin mistrafficking is caused by the lack of 11-cis retinal.

8 tly folded rhodopsin state by the binding of 11-cis retinal.

9 lium (RPE) visual cycle produces exclusively 11-cis retinal.

10 uter segments of Rpe65(-/-) mice, which lack 11-cis retinal.

11 RPE65 is essential for the generation of 11-cis retinal.

12 , opsin, covalently linked to a chromophore, 11-cis retinal.

13 of restoring functional cones with exogenous 11-cis retinal.

14 apoprotein opsin and the chromophore ligand 11-cis-retinal.

15 cone inner segments, where it is oxidized to 11-cis-retinal.

16 wed by opsin-catalyzed isomerization of free 11-cis-retinal.

17 , and high affinity of opsin apoproteins for 11-cis-retinal.

18 photoisomerization of the visual chromophore 11-cis-retinal.

19 retina to regenerate the visual chromophore, 11-cis-retinal.

20 ng retinyl esters of the visual chromophore, 11-cis-retinal.

21 lved that recycles all-trans-retinal back to 11-cis-retinal.

22 ase catalyzing a key step in regeneration of 11-cis-retinal.

23 in mammalian COS1 cells and regenerated with 11-cis-retinal.

24 s in the formation of the visual chromophore 11-cis-retinal.

25 in,all-trans-retinal must be reisomerized to 11-cis-retinal.

26 s exacerbated in conditions of low levels of 11-cis-retinal.

27 inol, in accord with its higher affinity for 11-cis-retinal.

28 opsin, and the light-sensitive chromophore, 11-cis-retinal.

29 with dietary vitamin A, it is converted into 11-cis-retinal.

30 ry into the visual cycle for processing into 11-cis-retinal.

31 the retinoid binding pocket is occupied with 11-cis-retinal.

32 interfere with the ability of opsin to bind 11-cis-retinal.

33 nt conductance changes after incubation with 11-cis-retinal.

34 ting regeneration of the visual chromophore, 11-cis-retinal.

35 t mice, which do not produce the chromophore 11-cis-retinal.

36 aximally at 424 nm after reconstitution with 11-cis-retinal.

37 presence of 9-cis-retinal and the absence of 11-cis-retinal.

38 ystems expressed a protein that stably bound 11-cis-retinal.

39 ogenase in the RPE, RDH10, which can produce 11-cis-retinal.

40 is-aldehyde different from that reported for 11-cis-retinal.

41 Rho), consists of an opsin protein linked to 11-cis-retinal.

42 e., illumination of the prebound chromophore 11-cis-retinal.

43 to reduce the generation and utilization of 11-cis-retinal.

44 e binding domain 1 (NBD1) specifically bound 11-cis-retinal.

45 teraction between the apoprotein and ligand, 11-cis-retinal.

46 brates, through which the visual chromophore 11-cis-retinal (11-cis-RAL) is generated to maintain nor

47 that stabilizes its inverse agonist ligand, 11-cis-retinal (11CR), by a covalent, protonated Schiff

48 found that binding for the inverse agonist, 11-cis-retinal (11CR), slowed when the sample contained

49 d all-trans-retinal were required to produce 11-cis-retinal; 2) together with 11-cis-retinal, all-tra

50 ely 900 min(-)(1) microM(-)(1)), followed by 11-cis-retinal (450 min(-)(1) mM(-)(1)) and 9-cis-retina

51 as well as rod/cone photoreceptors, contains 11-cis-retinal (a vitamin A derivative) and light isomer

52 (A2) chromophore, and regenerating with the 11-cis-retinal (A1) chromophore in the same isolated rod

53 Only 11- cis-retinal acts as an inverse agonist to the opsin.

54 istrafficking in both models was arrested on 11-cis retinal administration.

55 h cone loss and rod response are restored by 11-cis retinal administration.

56 the outer segments proceeded normally after 11-cis-retinal administration.

57 n in the recycling of the visual chromophore 11-cis-retinal after photoisomerization by a bleaching l

58 to produce 11-cis-retinal; 2) together with 11-cis-retinal, all-trans-retinol was produced at a 1:1

59 became more sustained in the presence of an 11-cis-retinal analog.

60 have measured the effects of all -trans- and 11- cis-retinals and -retinols on the opsin's ability to

61 s defined by a deficiency in ability to bind 11-cis retinal and form rhodopsin.

62 Variants of rhodopsin, a complex of 11-cis retinal and opsin, cause retinitis pigmentosa (RP

63 ngs raise the hypothesis that in normal RPE, 11-cis retinal and/or 11-cis retinol stimulate the efflu

64 el system, we used the retinoid chromophores 11-cis-retinal and 9-cis-retinal to monitor each monomer

65 This rescue effect increased synthesis of 11-cis-retinal and 9-cis-retinal, a functional iso-chrom

66 intaining the ability to form a pigment with 11-cis-retinal and activate the G protein transducin in

67 ation sets the open state of the channel for 11-cis-retinal and all-trans-retinal, with positioning o

68 y photoaffinity labeling with 3-diazo-4-keto-11-cis-retinal and by high resolution mass spectrometric

69 pt synthesis of the opsin chromophore ligand 11-cis-retinal and cause Leber congenital amaurosis (LCA

70 for vision through continuous generation of 11-cis-retinal and clearance of all-trans-retinal, respe

71 ges upon photoisomerization of rCRALBP-bound 11-cis-retinal and demonstrated ligand-dependent conform

72 -induced retinal degeneration indicates that 11-cis-retinal and docosahexaenoic acid (DHA) levels wer

73 odopsin as follows: thermal isomerization of 11-cis-retinal and hydrolysis of the protonated Schiff b

74 d treatments of illuminated homogenates with 11-cis-retinal and hydroxylamine prior to the AMP-PNP in

75 y RDH can prevent the accumulation of excess 11-cis-retinal and its Schiff-base conjugate and the for

76 anolamine (PE), the Schiff-base conjugate of 11-cis-retinal and PE, from the lumen to the cytoplasmic

77 erase RPE65, thereby slowing regeneration of 11-cis-retinal and reducing production of retinaldehyde

78 e conversion of dietary all-trans-retinol to 11-cis-retinal and suggest that these cells are the clos

79 e vision because of the diminished supply of 11-cis-retinal and the accumulation of toxic, constituti

80 The chromophore of visual pigments is 11-cis-retinal and, thus, in its absence, opsin is not p

81 igments, a covalent bond between the ligand (11-cis-retinal) and receptor (opsin) is crucial to spect

82 This animal does not generate 11-cis retinal, and both cone loss and rod response are

83 h active metabolites: the visual chromophore 11-cis-retinal, and retinoic acids, which regulate gene

84 Production of the visual chromophore, 11-cis-retinal, and retinosome formation also were docum

85 The C4 template mutant was unable to bind 11-cis-retinal, and the presence of Asn310/Lys311 was re

86 bilized to replenish the visual chromophore, 11-cis-retinal, and their storage ensures proper visual

87 eller cells, which synthesize a precursor of 11-cis-retinal, are closely adjoined to the cone ER, so

88 cation-selective ion channel, which employs 11-cis retinal as its chromophore.

89 Vertebrate rhodopsin (Rh) contains 11-cis-retinal as a chromophore to convert light energy

90 of vision concerns the natural selection of 11-cis-retinal as the light-sensing chromophore in visua

91 lizes a covalently tethered inverse agonist (11-cis-retinal) as the native ligand.

92 Visual opsins bind 11-cis retinal at an orthosteric site to form rhodopsins

93 converted to 11- cis-retinol and oxidized to 11- cis-retinal before it is transported back to the pho

94 Intraperitoneal administrations of 11-cis retinal before P25 led to increased transport of

95 85A and WT opsins, however, have contrasting 11-cis retinal binding kinetics.

96 e mutant suffer from low expression and poor 11-cis retinal binding.

97 Significant differences in 11-cis-retinal binding affinities were observed between

98 This long lifetime of 11-cis-retinal binding was considered to be physiologica

99 rdination is critical for rhodopsin folding, 11-cis-retinal binding, and the stability of the chromop

100 ns in this domain resulted in attenuation of 11-cis-retinal binding.

101 ABCA4 and, in particular, the NBD1 domain in 11-cis-retinal binding.

102 11-cis-retinal binds to opsin and undergoes a light-driv

103 et-NH2), a potent and selective inhibitor of 11-cis-retinal biosynthesis, is a substrate for LRAT.

104 s for the phenomenal dark state stability of 11-cis-retinal bound to rhodopsin and its ultrafast phot

105 set blindness, and Rpe65-deficient mice lack 11-cis-retinal but overaccumulate alltrans-retinyl ester

106 re evaluated before and after treatment with 11-cis retinal by intraperitoneal injection.

107 Thus, 11-cis retinal by itself, as well as other agents that f

108 iate regeneration of the visual chromophore, 11-cis-retinal, by the visual cycle.

109 Early administration of 9- or 11-cis retinal can partially prevent cone loss, suggesti

110 but exogenous supplementation of the native 11-cis retinal chromophore can inhibit this degeneration

111 the G protein-coupled receptors in having an 11-cis retinal chromophore covalently bound to the prote

112 Here we show that isomerization of the 11-cis retinal chromophore generates strong steric inter

113 y to long-wavelength light is to replace the 11-cis retinal chromophore in photopigments with 11-cis

114 Isomerization of the 11-cis retinal chromophore in the visual pigment rhodops

115 The 11-cis retinal chromophore is tightly packed within the

116 Absorption of light by its 11-cis retinal chromophore leads to rapid photochemical

117 hotochemical isomerization of the melanopsin 11-cis retinal chromophore occur via a space-saving mech

118 he pigment epithelium, which synthesizes the 11-cis retinal chromophore used by rod and cone photorec

119 lly functional visual pigments that bind the 11-cis retinal chromophore, activate the G protein trans

120 e protonated Schiff base linkage between the 11-cis-retinal chromophore and opsin protein.

121 inal cytotoxicity is enhanced by lack of the 11-cis-retinal chromophore during rod outer segment deve

122 e assumed to be involved in the recycling of 11-cis-retinal chromophore in the visual cycle.

123 Light-induced isomerization of the 11-cis-retinal chromophore in the visual pigment rhodops

124 ation with other RDH isoforms to produce the 11-cis-retinal chromophore needed for vision.

125 e is a recycling system that replenishes the 11-cis-retinal chromophore of rhodopsin and cone pigment

126 o-cell recycling system that replenishes the 11-cis-retinal chromophore of rhodopsin and cone pigment

127 id cycle, the enzymatic pathway by which the 11-cis-retinal chromophore of rhodopsin is generated, th

128 al cycle, the enzymatic pathway by which the 11-cis-retinal chromophore of rhodopsin is generated.

129 ed when the absorption of light converts the 11-cis-retinal chromophore to its all-trans configuratio

130 enzyme in the visual cycle that provides the 11-cis-retinal chromophore to photoreceptors in vivo.

131 g the chromophore exchange rate of the bound 11-cis-retinal chromophore with free 9-cis-retinal from

132 , a cis,trans-geometric isomerization of the 11-cis-retinal chromophore, a vitamin A derivative bound

133 alternation of the protonated Schiff base of 11-cis-retinal chromophore, induced by N87Q mutation and

134 by the isomerization of their all-trans and 11-cis retinal chromophores, respectively.

135 le of Abca4 may include the translocation of 11-cis-retinal complexes across the disk membrane.

136 In absence of their natural ligand, 11-cis-retinal, cone opsin G-protein-coupled receptors f

137 uccessful opsin trafficking and that without 11-cis retinal, cones may degenerate because of opsin mi

138 he eyes was reduced by approximately 43% and 11-cis-retinal content in the eye was reduced by approxi

139 In contrast, 11-cis-retinal content, ERGs and retinal histology were

140 n inhibit this degeneration, suggesting that 11-cis retinal could be used as a therapeutic agent for

141 reveals that intradiscal loop E-2 covers the 11-cis-retinal, creating a "retinal plug." Recently, we

142 pathology is attributed to a combination of 11-cis-retinal deficiency and photoreceptor degeneration

143 t that cone opsins are the 'culprit' linking 11-cis-retinal deficiency to cone degeneration in LCA.

144 ore of all known visual pigments consists of 11-cis-retinal (derived from either vitamin A1 or A2) or

145 Administration of exogenous 11-cis retinal did not rescue retinal morphology or mark

146 essed in HEK293 cells and reconstituted with 11-cis-retinal displayed an absorption spectrum similar

147 nockout (Rpe65-/-) mouse, where synthesis of 11-cis-retinal does not occur, a minimal visual response

148 n rhodopsin or opsin levels upon addition of 11-cis retinal during opsin expression.

149 roviding a 7-membered ring, locked analog of 11-cis-retinal during expression of P23H opsin in vivo.

150 the low concentration of intracellular free 11-cis retinal, estimated to be only a tiny fraction (ap

151 of two pathways: 1) thermal isomerization of 11-cis-retinal followed by hydrolysis of Schiff base (SB

152 nction is due to the limited availability of 11-cis-retinal for rod pigment formation.

153 eactions which converts all-trans-retinal to 11-cis-retinal for the regeneration of visual pigments i

154 ivo rates of all-trans-retinal reduction and 11-cis-retinal formation during recovery from bleaching

155 ing wild-type mice, the RESTs participate in 11-cis-retinal formation.

156 Regeneration of 11-cis retinal from all-trans retinol in the retinal pig

157 cone-specific redox reaction that generates 11-cis-retinal from 11-cis-retinol in the carp retina.

158 tor cells depend completely on the output of 11-cis-retinal from adjacent retinal pigment epithelial

159 timate that this slow spontaneous release of 11-cis-retinal from Rho should result in 10(4) to 10(5)

160 Cone photoreceptors cells can use 11-cis-retinal from the RPE and from a second more poorl

161 n, melanopsin regeneration depends partly on 11-cis-retinal from the RPE, possibly imported via Mulle

162 ce of its retinal chromophore isomerization, 11-cis-retinal --> all-trans-retinal.

163 P23H rhodopsins containing 9- or 11-cis-retinal had blue-shifted absorption maxima and al

164 f the gecko and chameleon reconstituted with 11-cis-retinal had the wavelengths of maximal absorption

165 As a result of this mutation, 11-cis retinal has been converted to an agonist.

166 to synthesize the visual pigment chromophore 11-cis retinal; however, if these animals are reared in

167 delivery resulted in substantial amounts of 11-cis retinal in Rpe65-/- mice.

168 asuring the rate of thermal isomerization of 11-cis retinal in solution, we conclude that the observe

169 native melanopsin in vivo exclusively binds 11-cis retinal in the dark and that illumination causes

170 to regenerate the visual pigment chromophore 11-cis retinal in the dark enzymatically, unlike in all

171 their chromophore from all-trans retinol to 11-cis retinal in the pigment epithelium, adjacent to ph

172 nyl ester in the RPE and exhibit very little 11-cis retinal in the retina.

173 Light isomerizes 11-cis-retinal in a retinal rod and produces an active f

174 ogical studies showed that ligand binding of 11-cis-retinal in dark-adapted Rho was essentially irrev

175 Addition of 11-cis-retinal in lipid vesicles, which produces regener

176 5 and Rdh11 does not limit the production of 11-cis-retinal in mice.

177 d and cone cells prevent the accumulation of 11-cis-retinal in photoreceptor disk membranes in excess

178 DH activity in the RPE, but the formation of 11-cis-retinal in rdh5-/- mice suggests another enzyme(s

179 We also show that thermal isomerization of 11-cis-retinal in solution can be catalyzed by wild-type

180 he photoreceptor cells requires formation of 11-cis-retinal in the adjacent retinal pigment epitheliu

181 ults argue against age-related deficiency of 11-cis-retinal in the B6D2F1/J mouse rod visual cycle.

182 ence of an effective production mechanism of 11-cis-retinal in the cone inner segment to regenerate v

183 e HierDock by predicting the binding site of 11-cis-retinal in the crystal structure of bovine rhodop

184 r, these results suggest that the binding of 11-cis-retinal in the ER is important for normal folding

185 used HierDock to predict the binding site of 11-cis-retinal in the MembStruk-predicted structure of b

186 The oxidation of 11-cis-retinol to 11-cis-retinal in the retinal pigment epithelium (RPE) r

187 strate for production of visual chromophore (11-cis-retinal) in vertebrates.

188 he presence of the pharmacological chaperone 11-cis-retinal increase the folding efficiency and resul

189 ice and the reintroduction of rosettes after 11-cis retinal injections confirm that outer segments, w

190 Light transforms the inverse agonist 11-cis-retinal into the agonist all-trans-retinal, leadi

191 h by converting vitamin A1 (the precursor of 11-cis retinal) into vitamin A2 (the precursor of 11-cis

192 Regeneration of 11-cis retinal is essential for survival of cone photore

193 ignalling photon absorption, the chromophore 11-cis retinal is first isomerized to all-trans retinal,

194 of 11-cis to all-trans retinal happens when 11-cis retinal is in the binding pocket of rhodopsin.

195 retinal pigment epithelium is disrupted, and 11-cis retinal is not generated.

196 ation of the covalent bond between opsin and 11-cis retinal is reversible in darkness in amphibian re

197 Oxidation of 11-cis-retinol to 11-cis-retinal is accomplished by a family of enzymes te

198 11-cis-Retinal is bound to opsins, forming visual pigmen

199 To sustain vision, 11-cis-retinal is continuously regenerated from its all-

200 segment of the visual cycle in which excess 11-cis-retinal is converted to all-trans-retinol provide

201 Furthermore, the presence of 11-cis-retinal is essential for proper transport of seve

202 Regeneration of the chromophore 11-cis-retinal is essential for the generation of light-

203 On absorption of light, 11-cis-retinal is isomerized to all-trans-retinal, const

204 The binding pocket for the chromophore 11-cis-retinal is minimally altered as palmitate-deficie

205 onstant illumination, a continuous supply of 11-cis-retinal is needed.

206 11-cis-retinal is the light-sensitive component in rod a

207 Rho (rhodopsin; opsin plus 11-cis-retinal) is a prototypical G protein-coupled rece

208 Regeneration of the visual chromophore, 11-cis-retinal, is a critical step in restoring photorec

209 Regeneration of the visual chromophore, 11-cis-retinal, is a crucial step in the visual cycle re

210 cle protein required for the regeneration of 11-cis-retinal, is associated with reduced A2E accumulat

211 absorption of a photon, the covalently bound 11- cis-retinal isomerizes to the all- trans form, enabl

212 er 80%, KI/KI mice retinae retain comparable 11-cis-retinal levels with WT.

213 by gene is mutated and if the mutant reduced 11-cis-retinal levels.

214 Although essential for vision, 11-cis-retinal like all-trans-retinal is highly toxic du

215 d receptor (GPCR) that is activated when its 11-cis-retinal moiety is photoisomerized to all-trans re

216 Regeneration of the 11-cis-retinal occurs in an adjacent tissue and involves

217 sing a single chromophore, in either the A1 (11- cis-retinal) or A2 (11- cis-3,4-dehydroretinal) form

218 and opsin dominates the natural selection of 11-cis-retinal over other cis isomers in the dark state.

219 be able to produce at least 10 molecules of 11-cis-retinal per minute.

220 ll below the K(m), the rate of production of 11-cis-retinal per RPE65 molecule was approximately 10 m

221 evaluated the responses of these mutants to 11-cis-retinal pharmacological chaperone rescue or disul

222 ting of a protein, opsin, and a chromophore, 11-cis-retinal, play a key role in shaping the light res

223 riggered only upon P-opsin regeneration with 11-cis-retinal, precluding noise generated by opsin acti

224 gene (RPE65(rd12)) with and without systemic 11-cis-retinal pretreatment.

225 However, accelerated 11-cis-retinal production and increased susceptibility t

226 A deficiency in 11-cis-retinal production leads to congenital blindness

227 plasma membrane are essential components in 11-cis-retinal production.

228 ased electrographic signaling and endogenous 11-cis-retinal production.

229 ire substantial recycling of the chromophore 11-cis-retinal (RAL) for continued function.

230 ese changes can be attributed to the lack of 11-cis retinal rather than to some unknown function of R

231 e prolonged effect of Ret-NH2 on the rate of 11-cis-retinal recovery in vivo.

232 ithin-retinol acyltransferase (LRAT) disrupt 11-cis-retinal recycling and cause Leber congenital amau

233 However, the kinetics of 11-cis-retinal recycling during dark adaptation was not

234 Rho*-Gt(e), Rho(e)*-Gt(e), and 9-cis-retinal/11-cis-retinal regenerated Rho-Gt(e) complexes by sucros

235 0 in RPE cells (Rdh10 cKO) displayed delayed 11-cis-retinal regeneration and dark adaption after brig

236 absence of prRDH did not affect the rate of 11-cis-retinal regeneration or the decay of Meta II, the

237 Treatment with 11-cis retinal restored cone function, promoted outer se

238 Exogenously increased 11-cis-retinal restored F81Y S-opsin protein expression

239 plementation of Rpe65(-/-)Nrl(-/-) mice with 11-cis retinal resulted in their reoccurrence.

240 sitized; subsequent treatment with exogenous 11-cis retinal results in pigment regeneration and subst

241 in complexes regenerated with 9-cis-retinal/11-cis-retinal, Rho retains a conformation similar to Rh

242 The dark-state (2)H NMR structure of 11-cis-retinal shows torsional twisting of the polyene c

243 Pups were injected intraperitoneally with 11-cis retinal, starting at postnatal day (P)10, and wer

244 dehyde, and CRALBP inhibits the reduction of 11-cis-retinal stronger than the oxidation of 11-cis-ret

245 as do not have a cone-specific mechanism for 11-cis retinal synthesis and have potential significance

246 ithin-retinol acyltransferase (LRAT) disrupt 11-cis-retinal synthesis and cause Leber congenital amau

247 of rhodopsin to estimate the maximum rate of 11-cis-retinal synthesis in vivo.

248 of the visual cycle necessary for generating 11-cis-retinal that functions not only as a molecular sw

249 sed rod outer segments; however, it was only 11-cis-retinal that generated such fluorophores when add

250 est that lipofuscin originates from the free 11-cis-retinal that is continuously supplied to the rod

251 ithelium protein, is essential in generating 11-cis retinal, the chromophore for all opsins.

252 noid visual cycle essential for recycling of 11-cis retinal, the chromophore for visual pigments in b

253 ase that converts all-trans retinyl ester to 11-cis retinal, the chromophore for visual pigments in v

254 the visual cycle that converts vitamin A to 11-cis retinal, the chromophore of the rod and cone phot

255 strate that A2E inhibits the regeneration of 11-cis retinal, the chromophore of visual pigments, whic

256 suggested that a higher rate regeneration of 11-cis-retinal, the chromophore for visual pigments, is

257 Consistently, levels of 11-cis-retinal, the chromophore for visual pigments, wer

258 tebrate retina responsible for production of 11-cis-retinal, the chromophore of rhodopsin and cone pi

259 RPE65 knockouts fail to synthesize 11-cis-retinal, the chromophore of rhodopsin, and accumu

260 hese RPE65 antagonists block regeneration of 11-cis-retinal, the chromophore of rhodopsin, thereby de

261 RPE65 is essential for the biosynthesis of 11-cis-retinal, the chromophore of rhodopsin.

262 ial for the synthesis by isomerohydrolase of 11-cis-retinal, the chromophore of rod and cone opsins.

263 nzymatic pathway that continuously generates 11-cis-retinal, the chromophore of visual pigments in ro

264 aurosis, the retinoid cycle is disrupted and 11-cis-retinal, the chromophore of visual pigments, is n

265 Rpe65(-/-) mice are unable to produce 11-cis-retinal, the chromophore of visual pigments.

266 mutant opsin is effectively rescued by 9- or 11-cis-retinal, the native chromophore.

267 rocessing all-trans-retinol (vitamin A) into 11-cis-retinal, the visual chromophore.

268 Production of 11-cis-retinal, the visual pigment chromophore, was supp

269 ll-trans retinal must be converted back into 11-cis-retinal through a series of enzymatic steps known

270 cling of the chromophore of visual pigments, 11-cis-retinal, through the retinoid visual cycle is an

271 ges that are induced by the isomerization of 11-cis retinal to all-trans retinal leading to the fully

272 light to the all-trans form be replaced with 11-cis retinal to regenerate the visual pigment.

273 Administration of 9- or 11-cis retinal to Rpe65(-/-) mice 2 weeks of age increas

274 lude that delivery of the highly hydrophobic 11-cis retinal to the interior of rod photoreceptors app

275 onverted the unprotonated Schiff base-linked 11-cis-retinal to a protonated form.

276 governing vision: the photoisomerization of 11-cis-retinal to all-trans-retinal and the enzymatic re

277 merization of opsin-bound visual chromophore 11-cis-retinal to all-trans-retinal triggers phototransd

278 toisomerization of the rhodopsin chromophore 11-cis-retinal to all-trans-retinal.

279 is thought to provide a privileged supply of 11-cis-retinal to cones by using 11-cis-retinol generate

280 aldehyde-binding protein (CRALBP) chaperones 11-cis-retinal to convert opsin receptor molecules into

281 rods, cones use the photosensitive molecule 11-cis-retinal to detect light, and in constant illumina

282 by rhodopsin leads to photoisomerization of 11-cis-retinal to its all-trans isomer.

283 with the protonated Schiff base linking the 11-cis-retinal to Lys296.

284 central cone opsins must be regenerated with 11-cis-retinal to permit transport to the outer segments

285 tially to regenerate and continuously supply 11-cis-retinal to retinal photoreceptor cells.

286 ecent report on the in vivo role of ABCA4 in 11-cis-retinal transport.

287 Previous studies have shown that 11-cis retinal-treated mice lacking RPE65 and raised in

288 However, in this study the authors show that 11-cis retinal-treated Rpe65(-/-)Rho(-/-) mice raised in

289 ese uptake returned to normal (P>0.05) after 11-cis retinal treatment.

290 11-cis-retinal uptake and all-trans-retinal release were

291 inol is oxidized selectively in cones to the 11-cis-retinal used for pigment regeneration.

292 11-cis Retinal was introduced into Rpe65(-/-)Rho(-/-) mi

293 The 9- or 11-cis retinal was supplied by intraperitoneal injection

294 No 11-cis-retinal was detected in T(-/-) or Rpe65(-/-) mice

295 nd to be only slightly higher in energy than 11-cis-retinal, which provides strong evidence for the p

296 ng of the covalent linkage between opsin and 11-cis-retinal, which was overlooked in the electrophysi

297 A high proportion of C185A opsin binds 11-cis retinal with a slow rate that reflects a denature

298 ssess replacement of the missing chromophore 11-cis retinal with oral QLT091001 (synthetic 9-cis-reti

299 Here, we determine the consequences of 11-cis retinal withdrawal and supplementation on cone de

300 first-out processing of all-trans retinol to 11-cis retinal within normally functioning RPE.