ライフサイエンスコーパス: retinaldehyde

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

2 marily with accumulating retinol rather than retinaldehyde.

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

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

5 carotene oxygenase 1 yields two molecules of retinaldehyde.

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

7 enzyme catalyzing the generation of RA from retinaldehyde.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

32 broblasts exhibit reduced metabolism of both retinaldehyde and retinol.

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

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

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

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

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

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

39 3H]RA, [3H]14-hydroxy-4,14-retroretinol, [3H]retinaldehyde, and [3H]3,4-didehydroretinol, but this me

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

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

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

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

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

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

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

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

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

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

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

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

52 3 (DHRS3), which catalyzes the reduction of retinaldehyde back to retinol.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 11-cis-retinol is in a complex with cellular retinaldehyde-binding protein (CRALBP), providing a clea

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

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

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

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

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

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

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

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

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

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

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

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

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

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

93 Adducts of retinaldehyde (bisretinoids) form nonenzymatically in ph

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

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

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

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

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

99 1-cis to all-trans photoisomerization of the retinaldehyde chromophore in a rod or cone opsin-pigment

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

120 Retinaldehyde dehydrogenase (RALDH) activity was assesse

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

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

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

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

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

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

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

128 10 (Il-10) and vitamin A metabolizing enzyme retinaldehyde dehydrogenase 2 (Aldh1a2) and to suppress

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

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

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

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

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

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

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

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

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

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

139 Retinaldehyde dehydrogenase 2, a critical enzyme in reti

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

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

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

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

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

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

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

147 Retinaldehyde dehydrogenase II (RalDH2) converts retinal

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

170 2 and 1, respectively, and 61% identical to retinaldehyde dehydrogenase/eta-crystallin of elephant s

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

172 Retinaldehyde dehydrogenases (Aldhs), also known as alde

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

194 kedly decreased capacity to reduce exogenous retinaldehydes in vitro.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 The retinaldehyde reductase activity of RDH12 protects the c

210 The membrane-associated retinaldehyde reductase and retinol dehydrogenase activi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

225 3-fold in Adh1-/- mice (indicating defective retinaldehyde synthesis).

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

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

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

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

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

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

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

233 1.2.1.3) with activity for the oxidation of retinaldehyde to retinoic acid.

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

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

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

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

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

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

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

241 Amounts of retinaldehydes were determined by extraction and HPLC.

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

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

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

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

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

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

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