ライフサイエンスコーパス: retinaldehyde

1 f retinoic acid (the oxidation of retinol to retinaldehyde).

2 somerization of its chromophore to all-trans-retinaldehyde.

3 marily with accumulating retinol rather than retinaldehyde.

4 atalyzes oxidation of 9-cis-retinol to 9-cis-retinaldehyde.

5 (ADH1), an enzyme that oxidizes retinol into retinaldehyde.

6 cal apocarotenoid derivatives in addition to retinaldehyde.

7 genase 1 (BCO1), generating two molecules of retinaldehyde.

8 O1-mediated central cleavage, producing only retinaldehyde.

9 that may represent a mechanism for escorting retinaldehyde.

10 to the vitamin A-derived chromophore, 11-cis-retinaldehyde.

11 ooxygenase (BCMO1) converts beta-carotene to retinaldehyde.

12 carotene oxygenase 1 yields two molecules of retinaldehyde.

13 eta-carotene to the retinoic acid precursor, retinaldehyde.

14 enzyme catalyzing the generation of RA from retinaldehyde.

15 or cone-opsin pigment isomerizes its 11-cis-retinaldehyde (11-cis-RAL) chromophore to all-trans-reti

16 in quantum-catch due to depletion of 11-cis-retinaldehyde (11-cis-RAL).

17 n opsin visual pigment isomerizes its 11-cis-retinaldehyde (11cRAL) chromophore to all-trans-retinald

18 ents is the protonated Schiff base of 11-cis-retinaldehyde (11cRAL).

19 oncomitant with significantly reduced 11-cis-retinaldehyde (11cRAL).

20 at oxidize 11-cis-retinol (11cROL) to 11-cis-retinaldehyde (11cRAL).

21 nt protein opsin, which together with 11-cis retinaldehyde absorbs light and activates a G-protein ca

22 r, in both organs the major NAD(+)-dependent retinaldehyde activity copurified with the propionaldehy

23 Some NAD(+)-independent retinaldehyde activity in both organs was associated wit

24 s; in both organs the major NAD(+)-dependent retinaldehyde activity was associated with the E1 isozym

25 A small amount of NAD(+)-dependent retinaldehyde activity was associated with the E2 isozym

26 configuration and protects against unwanted retinaldehyde activity.

27 delayed dark adaptation, increased all-trans-retinaldehyde (all-trans-RAL) following light exposure,

28 correlated with elevated levels of all-trans-retinaldehyde (all-trans-RAL) in retina after a photoble

29 thesis of A2E: (i) condensation of all-trans-retinaldehyde (all-trans-RAL) with phosphatidylethanolam

30 dehyde (11-cis-RAL) chromophore to all-trans-retinaldehyde (all-trans-RAL), which dissociates after a

31 tene is cleaved exclusively by BCO1 to yield retinaldehyde and alpha-retinaldehyde, bypassing mitocho

32 riod of activation, opsin releases all-trans-retinaldehyde and becomes insensitive to light.

33 ased accumulation of the cytotoxic all-trans retinaldehyde and hypersusceptibility to light-induced p

34 ted with greatly diminished eyecup levels of retinaldehyde and is reversible if the mutants are maint

35 se relies on the presence of cis-isoforms of retinaldehyde and is selectively sensitive to short-wave

36 egulator of cardiometabolic fitness and that retinaldehyde and its generating enzyme ADH1 act as crit

37 gously expressed melanopsin apparently binds retinaldehyde and mediates photic activation of G protei

38 hotoreceptor outer segments (OS) that clears retinaldehyde and prevents formation of toxic bisretinoi

39 s been shown to slow the synthesis of 11-cis-retinaldehyde and regeneration of rhodopsin by inhibitin

40 While functioning as the precursor of retinaldehyde and retinoic acid, a growing body of evide

41 ction in the cells, increasing the levels of retinaldehyde and retinoic acid.

42 The remarkable increase in activity of retinaldehyde and retinol as a consequence of 4-oxo deri

43 broblasts exhibit reduced metabolism of both retinaldehyde and retinol.

44 trate access channel to discriminate between retinaldehyde and short-chain aldehydes.

45 ovided by a protonated Schiff base adduct of retinaldehyde and taurine (A1-taurine, A1T) that forms r

46 ese results, the regeneration rate of 11-cis-retinaldehyde and the recovery rate for rod light sensit

47 s were done to identify enzymes metabolizing retinaldehyde and their relationship to enzymes metaboli

48 pears to function as a flippase of all-trans-retinaldehyde and/or its derivatives across the membrane

49 The k(cat) values of RDH12 for retinaldehydes and C(9) aldehydes are similar, but the K

50 (-)(/)(-) mice exhibited decreased levels of retinaldehydes and retinyl esters, and elevated levels o

51 3H]RA, [3H]14-hydroxy-4,14-retroretinol, [3H]retinaldehyde, and [3H]3,4-didehydroretinol, but this me

52 lation of embryonic ATRA levels for retinol, retinaldehyde, and ATRA-oxidizing enzymes; however, the

53 little effect on the reduction of all-trans-retinaldehyde, and CRALBP inhibits the reduction of 11-c

54 itamin A mobilization, impaired oxidation of retinaldehyde, and increased destruction of retinoic aci

55 )-mutant embryos, dietary supplementation of retinaldehyde, and retinol dehydrogenase (RDH) activity

56 which catalyzes the oxidation of retinol to retinaldehyde, and two subunits of NADPH-dependent dehyd

57 th arrestins, melanopsin could use all-trans-retinaldehyde as a chromophore, which suggests that it m

58 Whereas the function of retinaldehyde as chromophore is conserved from bacteria

59 but not E2 isozyme) could utilize CRBP-bound retinaldehyde as substrate, a feature thought to be spec

60 n of a photon isomerizes 11cRAL to all-trans-retinaldehyde (atRAL), briefly activating the pigment be

61 inaldehyde (11cRAL) chromophore to all-trans-retinaldehyde (atRAL), which subsequently dissociates.

62 We conclude that retinaldehyde availability is an important level at whic

63 o-opsin involves the conversion of all-trans-retinaldehyde back to 11-cis-retinaldehyde via an enzyme

64 specific reductase that effectively converts retinaldehyde back to retinol, decreasing the rate of re

65 3 (DHRS3), which catalyzes the reduction of retinaldehyde back to retinol.

66 a also suggest that this new photopigment is retinaldehyde based.

67 in and the physiologically relevant cellular retinaldehyde binding protein (CRALBP) both stimulate 11

68 tions determine the function of the cellular retinaldehyde binding protein (CRALBP) in the rod visual

69 Cellular retinaldehyde binding protein (CRALBP) plays a crucial r

70 is dependent on the 11-cis-specific cellular retinaldehyde binding protein (CRALBP) present in Muller

71 However, in mice lacking the cellular retinaldehyde binding protein (CRALBP), cone spectral se

72 markers of Muller cells, including cellular retinaldehyde binding protein (CRALBP), glutamine synthe

73 Cellular retinol/retinaldehyde binding protein (CRBP I) was localized to

74 homeobox 2 (OTX2) to activate the RPE65 and retinaldehyde binding protein 1 (RLBP1) promoters and ac

75 determine whether regulatory elements of the retinaldehyde binding protein 1 (Rlbp1; formerly Cralbp)

76 ng a portion of the regulatory region of the retinaldehyde binding protein 1 gene for conditional Mul

77 cycle through its interaction with cellular retinaldehyde binding protein and therefore may be a tar

78 n interact with the promoter of the cellular retinaldehyde binding protein gene in the presence of re

79 ogy and increased the expression of cellular retinaldehyde binding protein, a marker of the different

80 Immunostaining with antibodies to cellular retinaldehyde-binding protein (CRALBP) and glutamine syn

81 e-binding protein beta 3 (GNB3) and cellular retinaldehyde-binding protein (CRALBP) antibodies showed

82 Cellular retinaldehyde-binding protein (CRALBP) carries 11-cis-re

83 Cellular retinaldehyde-binding protein (CRALBP) chaperones 11-cis

84 Cellular retinaldehyde-binding protein (CRALBP) functions in the

85 Cellular retinaldehyde-binding protein (CRALBP) is abundantly exp

86 ol-binding protein (CRBP) type I or cellular retinaldehyde-binding protein (CRALBP) suggests that RDH

87 (EAAT1), glutamate synthetase (GS), cellular retinaldehyde-binding protein (CRALBP), and peanut agglu

88 , encoding the visual cycle protein cellular retinaldehyde-binding protein (CRALBP), cause an autosom

89 itive reactivity with antibodies to cellular retinaldehyde-binding protein (CRALBP), cytokeratin, and

90 n of carbonic anhydrase II (CA-II), cellular retinaldehyde-binding protein (CRALBP), glial fibrillary

91 n of carbonic anhydrase II (CA-II), cellular retinaldehyde-binding protein (CRALBP), glial fibrillary

92 l fibrillary acidic protein (GFAP), cellular retinaldehyde-binding protein (CRALBP), interphotorecept

93 11-cis-retinol is in a complex with cellular retinaldehyde-binding protein (CRALBP), providing a clea

94 he mRNA expression of FGFR1, FGFR2, cellular retinaldehyde-binding protein (CRALBP), RPE65, and heme

95 Cellular retinaldehyde-binding protein (CRALBP), transcribed from

96 l fibrillary acidic protein (GFAP), cellular retinaldehyde-binding protein (CRALBP), vimentin, and al

97 associated with RGR and enhanced by cellular retinaldehyde-binding protein (CRALBP), which binds the

98 acidic protein (GFAP)-specific and cellular retinaldehyde-binding protein (CRALBP)-specific antibodi

99 or absence of purified recombinant cellular retinaldehyde-binding protein (CRALBP).

100 Mutations in the cellular retinaldehyde-binding protein (CRALBP, encoded by RLBP1)

101 strophy caused by biallelic mutations in the retinaldehyde-binding protein 1 (RLBP1) gene of the visu

102 Mutations in retinaldehyde-binding protein 1 (RLBP1), encoding the vi

103 ize markers for Muller's cells (vimentin and retinaldehyde-binding protein 1), photoreceptors (L-M op

104 Genetic knockout of Des1 (degs1) or retinaldehyde-binding protein 1b (rlbp1b) did not elimin

105 Apo-cellular retinaldehyde-binding protein probably exerts its effect

106 Cellular retinaldehyde-binding protein was present up to day 7 in

107 The RLBP1 gene encodes the 36 kDa cellular retinaldehyde-binding protein, CRALBP, a soluble retinoi

108 Finally, the cellular retinaldehyde-binding protein-induced isomerization of a

109 assing RLBP1, the gene encoding the cellular retinaldehyde-binding protein.

110 only occurs in the presence of apo-cellular retinaldehyde-binding protein.

111 homologous to the gene encoding the cellular retinaldehyde-binding protein.

112 retinol acyltransferase (LRAT), and cellular retinaldehyde-binding protein.

113 isomerase and in mice deficient in cellular retinaldehyde-binding protein; in these models the produ

114 Adducts of retinaldehyde (bisretinoids) form nonenzymatically in ph

115 inaldehyde, which is isomerized to all-trans-retinaldehyde by absorption of a photon.

116 zymatic reactions: oxidation of retinol into retinaldehyde by alcohol dehydrogenases (ADHs) or retino

117 tivity requires chemical re-isomerization of retinaldehyde by an enzymatic pathway called the visual

118 oduction, beta,beta-carotene is converted to retinaldehyde by beta,beta-carotene monooxygenase 1 (Bcm

119 These data demonstrate that the reduction of retinaldehyde by DHRS3 is critical for preventing format

120 r the conversion of dietary beta-carotene to retinaldehyde by the enzyme BCO1.

121 ely by BCO1 to yield retinaldehyde and alpha-retinaldehyde, bypassing mitochondrial processing.

122 1-cis to all-trans photoisomerization of the retinaldehyde chromophore in a rod or cone opsin-pigment

123 perception is absorption of a photon by the retinaldehyde chromophore of an opsin pigment in a rod o

124 g of cone opsins due to impaired delivery of retinaldehyde chromophore, which functions as a chaperon

125 g a G protein-coupled receptor and an 11-cis-retinaldehyde chromophore.

126 igment, inducing isomerization of its 11-cis-retinaldehyde chromophore.

127 ces 11-cis to all-trans isomerization of its retinaldehyde chromophore.

128 t, which induces isomerization of its 11-cis-retinaldehyde chromophore.

129 ces 11-cis to all-trans isomerization of its retinaldehyde chromophore.

130 cone visual pigments and is able to bind the retinaldehyde chromophore.

131 hotoisomerization of an opsin-coupled 11-cis-retinaldehyde chromophore.

132 fold in Raldh1-/- mice (indicating defective retinaldehyde clearance) and decreased 3-fold in Adh1-/-

133 y different molecular mechanisms: the 11-cis-retinaldehydes combine with opsin to form the universal

134 ehyde-induced cell death, especially at high retinaldehyde concentrations, and this protective effect

135 of 11-cis-retinal and reducing production of retinaldehyde condensation byproducts that may be involv

136 activity of DHRS3 and the lack of changes in retinaldehyde conversion to retinol and retinoic acid in

137 because competition between acetaldehyde and retinaldehyde could result in abnormalities associated w

138 The intracellular enzyme retinaldehyde dehydrogenase (ALDH) provides resistance t

139 Here, we observed that among DCs, retinaldehyde dehydrogenase (ALDH1), which catalyzes the

140 , PPARgamma was crucial for the induction of retinaldehyde dehydrogenase (aldh1a2) selectively in CD1

141 , basic fibroblast growth factor (bFgf), and retinaldehyde dehydrogenase (Aldh1a2) was decreased and

142 it is concluded that in the human organism, retinaldehyde dehydrogenase (coded for by raldH1 gene) a

143 lterations in gene expression in C57Bl/6 and retinaldehyde dehydrogenase (RALDH) 1 knockout (KO) mice

144 Retinaldehyde dehydrogenase (RALDH) activity was assesse

145 hing on the RA signal involves the synthetic retinaldehyde dehydrogenase (RALDH) enzymes and it is cu

146 and we measured expression of cytokines and retinaldehyde dehydrogenase (RALDH) enzymes in ileum sam

147 re were carried out to identify and localize retinaldehyde dehydrogenase (RALDH) expression in postna

148 This was explored by using retinaldehyde dehydrogenase (Raldh)2-/- mouse embryos la

149 the skeletal phenotype of mice deficient in retinaldehyde dehydrogenase 1 (Aldh1a1), the enzyme resp

150 o, mice lacking the Rald-catabolizing enzyme retinaldehyde dehydrogenase 1 (Raldh1) resisted diet-ind

151 was absent in hepatocytes from mice lacking retinaldehyde dehydrogenase 1, the enzyme catalyzing the

152 10 (Il-10) and vitamin A metabolizing enzyme retinaldehyde dehydrogenase 2 (Aldh1a2) and to suppress

153 g macrophages, upregulated the expression of retinaldehyde dehydrogenase 2 (aldh1a2), which is key fo

154 ndered RA-deficient via targeted deletion of retinaldehyde dehydrogenase 2 (Raldh2(-/-)), the enzyme

155 Among them we show that retinaldehyde dehydrogenase 2 (RALDH2) and lipocalin-typ

156 pendent on retinoic acid (RA) synthesized by retinaldehyde dehydrogenase 2 (Raldh2) expressed proxima

157 ds to the endogenous synthesis of RA through retinaldehyde dehydrogenase 2 (Raldh2) in NG2 cells and

158 n that retinoic acid (RA) synthesized by the retinaldehyde dehydrogenase 2 (RALDH2) is required in fo

159 and progenitor/stem biology using the mouse retinaldehyde dehydrogenase 2 (Raldh2) knockout model.

160 ile in mDCs, including the gene that encodes retinaldehyde dehydrogenase 2 (RALDH2), a rate-limiting

161 rafish mutant neckless (nls), which disrupts retinaldehyde dehydrogenase 2 (raldh2), and in embryos t

162 yos deficient for the RA-synthesizing enzyme retinaldehyde dehydrogenase 2 (RALDH2), if rescued from

163 sis of RA-deficient foreguts from a genetic [retinaldehyde dehydrogenase 2 (Raldh2)-null] and a pharm

164 xd10 and the retinoic acid synthetic enzyme, retinaldehyde dehydrogenase 2 (RALDH2).

165 Retinaldehyde dehydrogenase 2, a critical enzyme in reti

166 y on RA generated in nearby stromal cells by retinaldehyde dehydrogenase 2, an enzyme required for mo

167 The retinaldehyde dehydrogenase 3 (Raldh3) gene encodes a ma

168 of the retinoic acid (RA) synthesis enzyme, retinaldehyde dehydrogenase 3 (Raldh3, also known as Ald

169 RA from both retinol and retinal, contains a retinaldehyde dehydrogenase activity for the second step

170 t expressing the vitamin A-converting enzyme retinaldehyde dehydrogenase and specialized in forkhead

171 s through retinoic acid and the induction of retinaldehyde dehydrogenase enzymes.

172 The mRNA levels of retinaldehyde dehydrogenase family 1 gene (Raldh1) were

173 Retinaldehyde dehydrogenase II (RalDH2) converts retinal

174 acid span in the substrate access channel in retinaldehyde dehydrogenase II is disordered, whereas in

175 s in either the cellular source of RA or the retinaldehyde dehydrogenase involved in RA synthesis.

176 Identification of ALDH6 as the retinaldehyde dehydrogenase present in normal human brea

177 plexus, which expresses the RA-synthesizing retinaldehyde dehydrogenase RALDH-2, is likely to repres

178 ldehyde dehydrogenase Aldh1a1, also known as retinaldehyde dehydrogenase Raldh1, plays a dominant rol

179 Retinaldehyde dehydrogenase type 2 (RALDH-2) is a major

180 e VAD-atRA-supported rat embryo model and in retinaldehyde dehydrogenase type 2 (RALDH2) mutant mice.

181 xpress the retinoic acid metabolizing enzyme retinaldehyde dehydrogenase type 2 and interleukin-10 (I

182 our results demonstrate a conserved role for retinaldehyde dehydrogenase type 2 in patterning the pos

183 lock in embryonic development that occurs in retinaldehyde dehydrogenase type 2 null mutant mice, and

184 ss, and present evidence that it inactivates retinaldehyde dehydrogenase type 2, an enzyme involved i

185 ) DCs was required for optimal expression of retinaldehyde dehydrogenase, a key enzyme for retinoic a

186 n of aldehyde dehydrogenase 1, also known as retinaldehyde dehydrogenase, by hematopoietic stem cells

187 enzyme mainly responsible for RA synthesis, retinaldehyde dehydrogenase, is expressed by radial glia

188 a cDNA encoding a novel dehydrogenase, named retinaldehyde dehydrogenase-2 (RALDH-2).

189 Limb RA synthesis is under the control of retinaldehyde dehydrogenase-2 (Raldh2) expressed in the

190 e analyzed initiation of lung development in retinaldehyde dehydrogenase-2 (Raldh2) null mice, a mode

191 d the hindbrain from the RA synthetic enzyme retinaldehyde dehydrogenase-2 (RALDH2) present in the su

192 or RA production during early embryogenesis, retinaldehyde dehydrogenase-2 (Raldh2), was expressed in

193 on or targeted disruption of the RA synthase retinaldehyde dehydrogenase-2 in other vertebrates.

194 ing gradients of retinoic acid (generated by retinaldehyde dehydrogenase-2; Raldh2) anteriorly and fi

195 pha and abundant expression of TGF-beta2 and retinaldehyde dehydrogenase.

196 2 and 1, respectively, and 61% identical to retinaldehyde dehydrogenase/eta-crystallin of elephant s

197 Wilms' Tumor transcription factor (WT1) and retinaldehyde-dehydrogenase2 (RALDH2).

198 Retinaldehyde dehydrogenases (Aldhs), also known as alde

199 It is synthesized by two retinaldehyde dehydrogenases (RALDH) present in both Ser

200 RA is synthesized by dedicated enzymes, the retinaldehyde dehydrogenases (RALDH), and binds to and a

201 expression of the RA synthetic enzymes, the retinaldehyde dehydrogenases (RALDH).

202 hain dehydrogenase/reductase gene family and retinaldehyde dehydrogenases (Raldh).

203 s produced by three different enzymes called retinaldehyde dehydrogenases (RALDH1, RALDH2 and RALDH3)

204 screte regions of the embryonic eye by three retinaldehyde dehydrogenases (RALDHs) displaying distinc

205 the phagocytosis-related ABCA1, and that of retinaldehyde dehydrogenases leading to the synthesis of

206 The synthesis is mediated by retinaldehyde dehydrogenases which convert some of the c

207 As the eye contains high levels of retinaldehyde dehydrogenases, and as the oxidation of re

208 conversion of retinal to RA, is performed by retinaldehyde dehydrogenases.

209 bstrate, a feature thought to be specific to retinaldehyde dehydrogenases.

210 trans-retinol or the oxidation of retinol to retinaldehyde depending on substrate and cofactor availa

211 In the presence of residual retinaldehyde-derived species present in membranes treat

212 eriod of activation, the resulting all-trans-retinaldehyde dissociates from the opsin apoprotein rend

213 Chemical side reactions of retinaldehyde during the recycling process can generate

214 id biosynthesis, the oxidation of retinol to retinaldehyde, during embryogenesis and in adulthood hav

215 ole for RDH10: in the biosynthesis of 11-cis-retinaldehyde for vision as well as the biosynthesis of

216 tinoids serve two main functions in biology: retinaldehyde forms the chromophore bound to opsins, and

217 igment epithelium 65 (RPE65), to form 11-cis-retinaldehyde from carotenoid substrates, whereas invert

218 27C1 directly accepts all-trans retinol and retinaldehyde from CRBP-1 and all-trans retinoic acid fr

219 ains bound, it is released as free all-trans retinaldehyde from illuminated vertebrate rhodopsin.

220 This is the first report of CRBP-bound retinaldehyde functioning as substrate for aldehyde dehy

221 tamin A is understood in substantial detail: retinaldehyde functions as the universal chromophore in

222 ly contributes to the reduction of all-trans-retinaldehyde; however, at saturating concentrations of

223 so essential for the oxidation of retinol to retinaldehyde in vivo Mice with targeted knockout of the

224 the observed relationship between the SAs of retinaldehydes in the retina and of RPE retinyl ester is

225 kedly decreased capacity to reduce exogenous retinaldehydes in vitro.

226 se activity of RDH12 protects the cells from retinaldehyde-induced cell death, especially at high ret

227 he main ALDH1 isozyme known to oxidize 9-cis retinaldehyde into 9-cis retinoic acid, which can regula

228 inol dehydrogenases (RDHs); and oxidation of retinaldehyde into RA by aldehyde dehydrogenases family

229 ation of Aldh1a.2 that irreversibly converts retinaldehyde into RA.

230 hyde dehydrogenases, and as the oxidation of retinaldehyde is an irreversible reaction, RA production

231 etarhodopsin to apo-opsin and free all-trans-retinaldehyde is faster with Pro347Ser-substituted rhodo

232 The majority of retinaldehyde is further metabolized to retinol (vitamin

233 ll cytosolic binding protein for retinol and retinaldehyde, is specifically restricted to preadipocyt

234 RA production is facilitated by retinaldehyde isoform-2 (RALDH2) preferentially expresse

235 e clearance pathway (oxidation of retinol to retinaldehyde), it is unknown what controls the second s

236 To restore light sensitivity, the all-trans-retinaldehyde must be chemically re-isomerized by an enz

237 ARE) was compared to the localization of the retinaldehyde-oxidizing dehydrogenase RALDH2, the earlie

238 Mechanistically, we found that the ADH1/retinaldehyde pathway works by driving PGC-1a nuclear tr

239 Furthermore, treatment with retinaldehyde prevented pCF remodeling in these animals.

240 and characterization of enzymes metabolizing retinaldehyde, propionaldehyde, and octanaldehyde from f

241 d Aldh1a3 expression, limiting conversion of retinaldehyde (Rald) to RA.

242 ases, are rate-limiting enzymes that convert retinaldehyde (Rald) to retinoic acid.

243 noic acid (ATRA) and its precursor all trans retinaldehyde (Rald), exhibit distinct and divergent tra

244 Retinoic acid is formed solely from retinaldehyde (Rald), which in turn is derived from vita

245 the amount of increase depending on the CRBP/retinaldehyde ratio.

246 in Rbp4(-/-) mice, we determined that 11-cis-retinaldehyde reached levels that were ~60% of WT at 4 m

247 The retinaldehyde reductase activity of RDH12 protects the c

248 The membrane-associated retinaldehyde reductase and retinol dehydrogenase activi

249 Herein, we investigate the role of the retinaldehyde reductase Dhrs3 in embryonic retinoid meta

250 uctase 3 (DHRS3) is thought to function as a retinaldehyde reductase that controls the levels of all-

251 ellular matrix communication, as well as the retinaldehyde reductase, DHRS3, a crucial retinol homeos

252 in living cells, RDH12 acts exclusively as a retinaldehyde reductase, shifting the retinoid homeostas

253 ole as a physiologically important all-trans-retinaldehyde reductase.

254 dizing enzymes; however, the contribution of retinaldehyde reductases to ATRA metabolism is not compl

255 ch convert some of the chromophore all-trans retinaldehyde, released from bleached rhodopsin, into RA

256 nol with much higher affinity than all-trans-retinaldehyde, restricts the oxidation of all-trans-reti

257 nm (UVA light) in the presence of all-trans-retinaldehyde results in photooxidative cytotoxicity.

258 Oxidation of retinol via retinaldehyde results in the formation of the essential

259 root clock, we used a chemical reporter for retinaldehyde (retinal)-binding proteins.

260 ted IFN-gamma synthesis effectively, whereas retinaldehyde, retinol, and retinyl acetate did not.

261 The retinaldehyde-RGR conjugate at neutral pH favors the nea

262 The enzyme also reduces retinaldehydes, showing equal activity for all-trans-ret

263 ith a broader distribution than the mRNA for retinaldehyde-specific aldehyde dehydrogenase (zRalDH),

264 RS3 acts as a robust high affinity all-trans-retinaldehyde-specific reductase that effectively conver

265 ide-treated larvae following exogenous 9-cis-retinaldehyde supplementation.

266 3-fold in Adh1-/- mice (indicating defective retinaldehyde synthesis).

267 ydrogenase associated with the conversion of retinaldehyde (the main vitamin A metabolite) into retin

268 uctase that controls the levels of all-trans-retinaldehyde, the immediate precursor for bioactive all

269 ns-retinol, leads to the formation of 11-cis-retinaldehyde, the visual chromophore, and all-trans-ret

270 which is indispensable for the synthesis of retinaldehyde, the visual chromophore, and retinoic acid

271 sin requires chemical regeneration of 11-cis-retinaldehyde through an enzymatic pathway called the vi

272 quires thermal re-isomerization of all-trans-retinaldehyde to 11-cis-retinaldehyde via an enzyme path

273 n vitro catalyzes the reduction of all-trans-retinaldehyde to all-trans-retinol or the oxidation of r

274 raretinal visual cycle that supplies 11- cis-retinaldehyde to cone opsins.

275 what controls the second step (oxidation of retinaldehyde to RA).

276 1.2.1.3) with activity for the oxidation of retinaldehyde to retinoic acid.

277 the reduction of the RA precursor all-trans retinaldehyde to vitamin A; however, a developmental fun

278 itivity requires chemical reisomerization of retinaldehyde via a multistep enzyme pathway, called the

279 on of all-trans-retinaldehyde back to 11-cis-retinaldehyde via an enzyme pathway called the visual cy

280 ization of all-trans-retinaldehyde to 11-cis-retinaldehyde via an enzyme pathway called the visual cy

281 re abundant under conditions in which 11-cis-retinaldehyde was higher; this included black versus alb

282 After retinol dosing, serum retinaldehyde was increased 2.5-fold in Raldh1-/- mice (

283 r of the other naturally occurring retinoid, retinaldehyde, was 4-5-fold faster than transfer of reti

284 Significant levels of ((3)H)retinaldehydes were detected in the retinas of Rpe65(+/+

285 Amounts of retinaldehydes were determined by extraction and HPLC.

286 es A2PE, A2E, and A2PE-H(2), which form from retinaldehyde, were elevated in Pro347Ser transgenic mic

287 hodopsin results in its release of all-trans-retinaldehyde, which constitutes the first reactant in A

288 erproduction of retinoic acid from all-trans-retinaldehyde, which diffuses into the inner segments of

289 sorbing chromophore in most opsins is 11-cis-retinaldehyde, which is isomerized to all-trans-retinald

290 '-oxygenase (BCO1) converts beta-carotene to retinaldehyde, which is then oxidized to retinoic acid,

291 r cell outer segments by random reactions of retinaldehyde with phosphatidylethanolamine.

292 LDH-2 to be highly effective in oxidation of retinaldehyde, with no detectable activity on any other

293 CRBP to RALDH-2 increased RA synthesis from retinaldehyde, with the amount of increase depending on

294 that the primary amine of taurine forms with retinaldehyde would readily hydrolyze to release the ret