ライフサイエンスコーパス: ALDH1

1 ALDH1 mRNA was highly expressed in untreated rat liver,

2 ALDH1 transduction into peripheral blood human hematopoi

3 ALDH1 was also shown to be an early predictor of EC deve

4 ALDH1 was more efficient at oxidizing acetaldehyde, prop

5 ALDH1(+)CD44(+) cells are putative tumor-initiating cell

6 ALDH1(br) cells were enriched in ES-2 (1.3%), TOV-21G (1

7 1 x 10(4), 3 x 10(3), and 1 x 10(3) s-1 M-1 ALDH1-sulfone, ALDH1-sulfoxide, ALDH2-sulfone, and ALDH2

8 metric analysis of aldehyde dehydrogenase 1 (ALDH1) activity and the CD44(high)/CD24(low)/epithelial

9 Xs) also expressed aldehyde dehydrogenase 1 (ALDH1) and had a greater capacity to form spheroids and

10 wo human proteins, aldehyde dehydrogenase 1 (ALDH1) and quinone reductase 2 (QR2).

11 The role of aldehyde dehydrogenase 1 (ALDH1) as an ovarian cancer stem cell marker and its cli

12 like cells, reduce aldehyde dehydrogenase 1 (ALDH1) expression, and decrease mammosphere and progenit

13 cancer, but while aldehyde dehydrogenase 1 (ALDH1) has been suggested as a putative cancer stem cell

14 Aldehyde dehydrogenase 1 (ALDH1) has been suggested as a surrogate biomarker for c

15 Aldehyde dehydrogenase 1 (ALDH1) plays a major role in the biosynthesis of retinoi

16 Accordingly, aldehyde dehydrogenase 1 (ALDH1) was investigated as a possible marker for identif

17 A relatively rare aldehyde dehydrogenase 1 (ALDH1)-positive "stem cell-like" subpopulation of tumor

18 ll markers such as Aldehyde Dehydrogenase 1 (ALDH1).

19 markers including aldehyde dehydrogenase 1 (ALDH1).

20 evel of CD44v3 and aldehyde dehydrogenase-1 (ALDH1) expression.

21 vels of CD44v3 and aldehyde dehydrogenase-1 (ALDH1) expression.

22 These results support that a miR-140/ALDH1/SOX9 axis is critical to basal CSC self-renewal an

23 elium to mutant (APC) epithelium to adenoma, ALDH1(+) cells increased in number and became distribute

24 e ALDH1-positive lobules but not in adjacent ALDH1-negative lobules.

25 The second gene encodes a "non-lens" ALDH1 (ALDH1-nl) which is the predominant form expressed in liv

26 3189 blocks reconstitution of mixed ALDH1(+)/ALDH1(-) cultures indicating that BMP signaling may gove

27 H1 and ADH4), one SDR (RDH5), and two ALDHs (ALDH1 and RALDH2) all of which are conserved between hum

28 acter was restricted to cells that were also ALDH1(+), implying that only ALDH1(+) EMT cells had the

29 An ALDH1 T244S mutant was recombinantly expressed and was u

30 RA decreased expression of an ALDH1-CAT construct containing -2536 base pairs of DNA u

31 4, CD133, CD24, MSH1 (alias, Musashi-1), and ALDH1] and that this epigenetic profile can identify agg

32 Both ALDH1(br) and ALDH1(low) cells repopulated stem cell heterogeneity, fo

33 ls, as measured by the CSC markers CD133 and ALDH1 activity (Aldefluor).

34 f molecules such as CXCR4, IGFBP5, CD133 and ALDH1.

35 ment of the CD44(high)/CD24(low), CD133, and ALDH1 stem cell-like markers.

36 reduction of the pool of CD44(+)/CD24(-) and ALDH1 high breast cancer stem cells by threefold and two

37 presence of markers such as CD44, CD24, and ALDH1, with further characterisation using mammosphere a

38 xpressed oral CSC markers including CD44 and ALDH1 and showed increased PI3K pathway activation.

39 putative cancer stem cell markers, CD44 and ALDH1, increased resistance to chemotherapy drugs, enhan

40 OX9, and beta-CATENIN), of CSCs (CD44v6, and ALDH1), and the metastasis-associated gene signature, co

41 h BMI1, TWIST1, and DVL1 in mammospheric and ALDH1+ populations.

42 emboli of human IBC exhibited dual N3icd and ALDH1 immunoreactivities independently of molecular subt

43 ary compound sulforaphane decreased SOX9 and ALDH1, and reduced tumor growth in vivo.

44 Furthermore, we found that SOX9 and ALDH1, the most significantly activated stem-cell factor

45 Both ALDH1(br) and ALDH1(low) cells repopulated stem cell het

46 an Aldefluor assay to isolate ALDH1-bright (ALDH1(br)) cells from epithelial ovarian cancer cell lin

47 sistant phenotype was specifically caused by ALDH1 overexpression as shown by its reversion by disulf

48 in the number of blood vessels surrounded by ALDH1(high) or Bmi-1(high) cells (perivascular niches) c

49 ous expression decreased the number of CD133/ALDH1-positive cells present in the cell population.

50 4, and Sox2, and a high percentage of CD44(+)ALDH1(+) CSC in OSCC.

51 Ectopic Lin28B expression in CD44(-)ALDH1(-)/OSCC cells was sufficient to enhance Oct4/Sox2

52 In the ES-2 and CP70 cells, ALDH1(br) cells conferred more chemoresistance, and were

53 In this cohort, ALDH1 expression alone does not significantly predict ou

54 In disease progression, cytoplasmic ALDH1 expression showed a step-wise increase between end

55 LDH isoenzymes, the genes encoding cytosolic ALDH1 and mitochondrial ALDH2 and ALDH5 were disrupted i

56 ned an open reading frame encoding cytosolic ALDH1, with 500 amino acids, which was located on chromo

57 haracterized recombinant rat liver cytosolic ALDH1 and ALDH-PB.

58 electric focusing gels showed that cytosolic ALDH1 contributed 30 to 70% of the overall activity, dep

59 We expressed recombinant human cytosolic (ALDH1, high Km) and mitochondrial aldehyde dehydrogenase

60 ctants downregulated Oct4 and also decreased ALDH1 activity, another stem cell-associated factor, enh

61 ant of human class 1 aldehyde dehydrogenase (ALDH1) that was no longer inhibited by Mg(2+) ions but w

62 porter and increased aldehyde dehydrogenase (ALDH1), have been associated with these cells.

63 ytoplasmic (class 1) aldehyde dehydrogenase (ALDH1, EC 1.2.1.3) with activity for the oxidation of re

64 of expression of the aldehyde-dehydrogenase (ALDH1) gene in tumor cell lines in vitro, we tested whet

65 that among DCs, retinaldehyde dehydrogenase (ALDH1), which catalyzes the conversion of retinal to ATR

66 Detectable ALDH1 predicted better prognosis in both cohorts (P = 0.

67 One encodes ALDH1/eta-crystallin which, in addition to its very high

68 and diminishes the cancer stem cell-enriched ALDH1(+) population.

69 n the promoter regions of BCSC genes, except ALDH1.

70 hibitor daidzin for selectivity against five ALDH1/2 isoenzymes.

71 upon the selectivity toward one of the five ALDH1/2 isoenzymes, including compound 36, a selective i

72 their isolation by FACS using a fluorogenic ALDH1 substrate.

73 Using a multiplexed assay for ALDH1, CD44, and cytokeratin to measure the coexpression

74 /- 0.04 microM, and 0.12 +/- 0.02 microM for ALDH1, and 1.45 +/- 0.40 microM, 1.16 +/- 0.56, and 0.40

75 were classified as positive or negative for ALDH1 based on the detection threshold for quantitative

76 ough histologically normal, are positive for ALDH1 expression but are negative for the expression of

77 dings reveal an important conserved role for ALDH1 in retinoic acid synthesis in vivo, and demonstrat

78 Immunohistochemical staining for ALDH1 on a tissue microarray containing 84 epithelial ov

79 Consistent with the rate-limiting step for ALDH1 being changed from coenzyme dissociation to deacyl

80 ADH dissociation, the rate-limiting step for ALDH1, and enhanced deacylation, the rate-limiting step

81 insic drug resistance of BTICs is their high ALDH1 activity leading to inhibition of chemotherapy-ind

82 from patients revealed that cells with high ALDH1 activity have low ALDH1A1 acetylation and are capa

83 relatively abundant CD133(high)-ASCL1(high)-ALDH1(high) subpopulation with markedly enhanced tumorig

84 r samples revealed that patients with higher ALDH1 expression (>50%) had poor overall survival, compa

85 The homotetramer (ALDH1 or ALDH2) is a dimer of dimers (A-B + C-D).

86 We have cloned a full-length human ALDH1 cDNA and used retroviral vectors to transduce it i

87 re low Km values (microM) for retinal: human ALDH1 (72.2%), rat retinal dehydrogenase, type I (71.5%)

88 hough these processes were more efficient in ALDH1(br) cells.

89 erminal tail in ALDH3 that is not present in ALDH1 or 2.

90 ail in ALDH3, addition of different tails in ALDH1, and mutations of different residues located in th

91 ehyde dehydrogenase enzyme family, including ALDH1.

92 of FoxQ1 in MCF-7 and SUM159 cells increased ALDH1 activity and the CD49f(+)/CD24(-) fraction.

93 regulators, as well as a fivefold increased ALDH1 activity, a threefold enrichment for CD44(+)/CD24(

94 ALDH-PB is not merely an inducible ALDH1 isozyme; it is a distinct ALDH isozyme.

95 DATS administration inhibited ALDH1 activity in vivo in SUM159 xenografts.

96 We used an Aldefluor assay to isolate ALDH1-bright (ALDH1(br)) cells from epithelial ovarian c

97 ydrogenases (ALDHs): a constitutive isozyme (ALDH1) and a phenobarbital-inducible isozyme (ALDH-PB).

98 The second gene encodes a "non-lens" ALDH1 (ALDH1-nl) which is the predominant form expressed

99 class 1 ALDH, ALDH-PB does not function like ALDH1.

100 ver ALDH1 is the ortholog of mammalian liver ALDH1.

101 Rat liver ALDH1 had a high affinity for retinal (K(m) = 0.6 microM

102 We conclude that rat liver ALDH1 is the ortholog of mammalian liver ALDH1.

103 rofile characterized by CD44(+)/CD24(-/low), ALDH1, and most uniquely, CD133.

104 all survival, compared with those with lower ALDH1 (P = 0.004) and yielded an odds ratio of death of

105 of the aldehyde dehydrogenases, is the main ALDH1 isozyme known to oxidize 9-cis retinaldehyde into

106 her mammals which make use of the same major ALDH1 transcript in both ocular and non-ocular tissues.

107 hat ALDH-PB is the rat ortholog of mammalian ALDH1, and the identity of rat ALDH-PB is commonly inter

108 binding site than those of related mammalian ALDH1 enzymes with the cofactor bound in the "hydride tr

109 In contrast to mammalian ALDH1 and -2 and other cephalopod Omega-crystallins, whi

110 ding CD44(+)CD24(-) fractions, mammospheres, ALDH1(+) populations and side population cells.

111 s displaying the stem/progenitor cell marker ALDH1 and a decrease in cells expressing luminal epithel

112 similar to the established stem cell marker ALDH1.

113 express stem and/or progenitor cell markers ALDH1, LGR5, LEF1, CD133 and CK6B.

114 ative immunofluorescence was used to measure ALDH1 in 134 patients with NSCLC from Yale University an

115 We quantitatively measured ALDH1 in two large cohorts of patients with non-small ce

116 ly, LDN193189 blocks reconstitution of mixed ALDH1(+)/ALDH1(-) cultures indicating that BMP signaling

117 ntial determinant in the catalytic action of ALDH1.

118 ions affected only the NAD(+) activation of ALDH1.

119 The activity of ALDH1 was stimulated two- to fourfold by divalent cation

120 The use of a combination of ALDH1 with other stem cell markers may help define ovari

121 The effect of ALDH1 expression was independent of clinicopathologic fa

122 provide a basis for testing the efficacy of ALDH1 gene transduction to protect bone marrow cells fro

123 expression of the SNAI1 gene, enrichment of ALDH1(high) BTICs, self-renewal capacity, and chemoresis

124 bserved significantly elevated expression of ALDH1 in lung metastasis and MDR1/LDH-A expression in li

125 Thus, premature expression of ALDH1 stimulates premature synthesis of retinoic acid.

126 ion in lens, is also the predominant form of ALDH1 expressed in other parts of the eye.

127 collateral recruitment as the major form of ALDH1 expressed in other parts of the eye.

128 to determine the intensity and frequency of ALDH1 expression.

129 Inhibition of ALDH1 activity and/or mammosphere formation upon DATS tr

130 The inhibition of ALDH1 and activation of ALDH2 at pH 7.4 are due to their

131 TD cells are characterized by high levels of ALDH1 enzymatic activity, related to high-level expressi

132 retory endometrium showed very low levels of ALDH1, slightly higher expression was observed within th

133 plays a critical role in the maintenance of ALDH1+ tumor cells.

134 further demonstrated with an E399Q mutant of ALDH1 whose rate-limiting step had been changed from NAD

135 t only gives a view of a "natural mutant" of ALDH1 illustrating the adaptive conflict that can arise

136 inical problems associated with mutations of ALDH1, ALDH2, ALDH4, ALDH10 and succinic semialdehyde (S

137 Overexpression of ALDH1 by injection of Xenopus embryos with mRNAs encodin

138 positively correlated with the percentage of ALDH1+ tumor cells; this was further validated in an ind

139 raftment was correlated with the presence of ALDH1-positive CSCs, which predicted prognosis in patien

140 and in vivo studies show that the progeny of ALDH1(+)/CD90(-)/Ecad(-) cells residing in the adult mou

141 ells with high YAP1 and a high proportion of ALDH1(+).

142 Thus the gene recruitment of ALDH1/eta-crystallin as a structural protein in elephant

143 Additionally, a significant reduction of ALDH1, CD44 and Oct-3/4, key markers of pancreatic CSC w

144 (2+) ions on each individual kinetic step of ALDH1 and ALDH2.

145 gen/ITGA1 signaling promotes the survival of ALDH1-positive stem-like cells and cooperates with TGFbe

146 udy was to investigate the clinical value of ALDH1 expression in endometrial hyperplasia and to deter

147 that were also ALDH1(+), implying that only ALDH1(+) EMT cells had the ability to seed a new epithel

148 by CD44 positivity, CD24 negativity, and/or ALDH1 positivity in flow cytometric studies.

149 bit a basal-like CD44(high)/CD24(low) and/or ALDH1(high) phenotype with critical cancer stem-like fea

150 SCCHN cell lines overexpressing ALDH1 had high enzymatic activity.

151 The recombinant ALDH1 enzyme was found to be essentially NADP dependent,

152 ests that elevated hepatic RA down-regulates ALDH1 in a unique feedback pathway to control RA biosynt

153 r cells, and that let-7 negatively regulates ALDH1+ tumor cells.

154 to enhance CSC features (side population-SP, ALDH1+, and tumorspheres) and self-renewal markers NANOG

155 n by its reversion by disulfiram, a specific ALDH1 inhibitor.

156 10(3), and 1 x 10(3) s-1 M-1 ALDH1-sulfone, ALDH1-sulfoxide, ALDH2-sulfone, and ALDH2-sulfoxide, res

157 The results did not support ALDH1 alone as an ovarian cancer stem cell marker, but d

158 ld be a novel therapeutic strategy to target ALDH1+ cancer stem cells.

159 ncer stem cell marker, but demonstrated that ALDH1 is associated with CD44 expression, chemoresistanc

160 e we describe the first direct evidence that ALDH1 plays a physiological role in retinoic acid synthe

161 These findings indicate that ALDH1 overexpression is sufficient to induce cyclophosph

162 atory and retrospective study indicates that ALDH1 expression is associated with favorable outcome.

163 Here, we report that ALDH1(+)CD44(+)-HNC cells express reduced levels of miR1

164 Our results show that ALDH1 and QR2 are selective targets of the quinolines an

165 Immunostaining showed that ALDH1(+) cells are sparse and limited to the normal cryp

166 Confocal microscopy showed that ALDH1(high) and Bmi-1(high) stem cells are preferentiall

167 hich the RARalpha and C/EBPbeta activate the ALDH1 gene promoter through the RARE and C/EBP response

168 Among patients with adenocarcinoma, the ALDH1-negative group had shorter survival compared with

169 ' and directly adjacent to the RARE, and the ALDH1 gene is down-regulated in C/EBPbeta-null mouse liv

170 also enhanced mammosphere formation and the ALDH1+ population in estrogen receptor-positive mammary

171 elf-renewal of ER-MC cells and increased the ALDH1+ population, whereas siRNA-mediated depletion of A

172 etermine the mechanism of suppression of the ALDH1 gene by RA, transactivation studies were carried o

173 Overexpression of the ALDH1 gene resulted in a significant increases in cyclop

174 showed a diminution to the stability of the ALDH1 mutants.

175 the unique and overlapping functions of the ALDH1/2 isoenzymes.

176 ignificantly reduced cell proliferation, the ALDH1(+) and CD44(+)/CD24(-) CSC subpopulations, and mam

177 s diminished oncogenic activity, reduced the ALDH1-positive cell population, and increased reactive o

178 protein (C/EBPbeta) also transactivates the ALDH1 gene promoter through a CCAAT box located 3' and d

179 receptor alpha (RARalpha) transactivates the ALDH1 gene promoter through a complex with an RA respons

180 isoforms in endometrial cancer, of which the ALDH1 isoforms collectively constituted the largest grou

181 cell organization of breast cancer with the ALDH1-positive CSCs constituting the tumorigenic cell po

182 group had shorter survival compared with the ALDH1-positive group in the Yale cohort (P = 0.00001), b

183 in indicates that diversification within the ALDH1/2/5/6 gene cluster occurred during the Neoproteroz

184 rozygosity for BRCA1 was documented in these ALDH1-positive lobules but not in adjacent ALDH1-negativ

185 Thus, ALDH1 seems to be a specific marker for identifying, iso

186 nfer tumor-initiating properties in non-TICs/ALDH1(-)CD44(-)-HNC and this effect could be abrogated b

187 ression or ADAM17 overexpression in non-TICs/ALDH1(-)CD44(-)-HNC cells increased expression and secre

188 medium from Spg-miR145-transfected non-TICs/ALDH1(-)CD44(-)-HNC cells was sufficient to confer tumor

189 tumor-initiating characteristics in non-TICs/ALDH1(-)CD44-negative HNC cells.

190 many other mammals, elephant shrews have two ALDH1 genes.

191 induced LP CD103(+) DCs to generate ATRA via ALDH1 activity.

192 retinoic acid occurs during neurulation when ALDH1 is first expressed.

193 tumor cell lines in vitro, we tested whether ALDH1 overexpression could directly induce cyclophospham

194 Unlike breast cancer, in which ALDH1 expression predicts poor outcome, in NSCLC our exp

195 and 1.17-fold, respectively), compared with ALDH1(low) cells.

196 expression was significantly correlated with ALDH1 expression in a cohort of ER-MC patients.

197 of rat ALDH-PB is commonly interchanged with ALDH1.

198 Xenopus ALDH1 was not expressed at blastula and gastrula stages,

199 h mRNAs encoding the mouse, chick or Xenopus ALDH1 homologs induced high levels of retinoic acid dete

200 The Xenopus ALDH1 gene was cloned and shown to be highly conserved w