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1 ALDH1 mRNA was highly expressed in untreated rat liver,
2 ALDH1 transduction into peripheral blood human hematopoi
3 ALDH1 was more efficient at oxidizing acetaldehyde, prop
4 ALDH1(+)CD44(+) cells are putative tumor-initiating cell
5 ALDH1(br) cells were enriched in ES-2 (1.3%), TOV-21G (1
6 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
7 metric analysis of aldehyde dehydrogenase 1 (ALDH1) activity and the CD44(high)/CD24(low)/epithelial
8 Xs) also expressed aldehyde dehydrogenase 1 (ALDH1) and had a greater capacity to form spheroids and
11 like cells, reduce aldehyde dehydrogenase 1 (ALDH1) expression, and decrease mammosphere and progenit
15 A relatively rare aldehyde dehydrogenase 1 (ALDH1)-positive "stem cell-like" subpopulation of tumor
21 elium to mutant (APC) epithelium to adenoma, ALDH1(+) cells increased in number and became distribute
23 The second gene encodes a "non-lens" ALDH1 (ALDH1-nl) which is the predominant form expressed in liv
24 3189 blocks reconstitution of mixed ALDH1(+)/ALDH1(-) cultures indicating that BMP signaling may gove
25 H1 and ADH4), one SDR (RDH5), and two ALDHs (ALDH1 and RALDH2) all of which are conserved between hum
26 acter was restricted to cells that were also ALDH1(+), implying that only ALDH1(+) EMT cells had the
29 4, CD133, CD24, MSH1 (alias, Musashi-1), and ALDH1] and that this epigenetic profile can identify agg
34 reduction of the pool of CD44(+)/CD24(-) and ALDH1 high breast cancer stem cells by threefold and two
35 presence of markers such as CD44, CD24, and ALDH1, with further characterisation using mammosphere a
37 putative cancer stem cell markers, CD44 and ALDH1, increased resistance to chemotherapy drugs, enhan
39 emboli of human IBC exhibited dual N3icd and ALDH1 immunoreactivities independently of molecular subt
43 an Aldefluor assay to isolate ALDH1-bright (ALDH1(br)) cells from epithelial ovarian cancer cell lin
44 sistant phenotype was specifically caused by ALDH1 overexpression as shown by its reversion by disulf
45 ous expression decreased the number of CD133/ALDH1-positive cells present in the cell population.
50 LDH isoenzymes, the genes encoding cytosolic ALDH1 and mitochondrial ALDH2 and ALDH5 were disrupted i
51 ned an open reading frame encoding cytosolic ALDH1, with 500 amino acids, which was located on chromo
53 electric focusing gels showed that cytosolic ALDH1 contributed 30 to 70% of the overall activity, dep
54 We expressed recombinant human cytosolic (ALDH1, high Km) and mitochondrial aldehyde dehydrogenase
55 ctants downregulated Oct4 and also decreased ALDH1 activity, another stem cell-associated factor, enh
56 ant of human class 1 aldehyde dehydrogenase (ALDH1) that was no longer inhibited by Mg(2+) ions but w
58 ytoplasmic (class 1) aldehyde dehydrogenase (ALDH1, EC 1.2.1.3) with activity for the oxidation of re
59 of expression of the aldehyde-dehydrogenase (ALDH1) gene in tumor cell lines in vitro, we tested whet
60 that among DCs, retinaldehyde dehydrogenase (ALDH1), which catalyzes the conversion of retinal to ATR
66 upon the selectivity toward one of the five ALDH1/2 isoenzymes, including compound 36, a selective i
69 /- 0.04 microM, and 0.12 +/- 0.02 microM for ALDH1, and 1.45 +/- 0.40 microM, 1.16 +/- 0.56, and 0.40
70 were classified as positive or negative for ALDH1 based on the detection threshold for quantitative
71 ough histologically normal, are positive for ALDH1 expression but are negative for the expression of
72 dings reveal an important conserved role for ALDH1 in retinoic acid synthesis in vivo, and demonstrat
74 Consistent with the rate-limiting step for ALDH1 being changed from coenzyme dissociation to deacyl
75 ADH dissociation, the rate-limiting step for ALDH1, and enhanced deacylation, the rate-limiting step
76 from patients revealed that cells with high ALDH1 activity have low ALDH1A1 acetylation and are capa
77 relatively abundant CD133(high)-ASCL1(high)-ALDH1(high) subpopulation with markedly enhanced tumorig
78 r samples revealed that patients with higher ALDH1 expression (>50%) had poor overall survival, compa
81 re low Km values (microM) for retinal: human ALDH1 (72.2%), rat retinal dehydrogenase, type I (71.5%)
84 ail in ALDH3, addition of different tails in ALDH1, and mutations of different residues located in th
87 regulators, as well as a fivefold increased ALDH1 activity, a threefold enrichment for CD44(+)/CD24(
91 ydrogenases (ALDHs): a constitutive isozyme (ALDH1) and a phenobarbital-inducible isozyme (ALDH-PB).
98 all survival, compared with those with lower ALDH1 (P = 0.004) and yielded an odds ratio of death of
99 her mammals which make use of the same major ALDH1 transcript in both ocular and non-ocular tissues.
100 hat ALDH-PB is the rat ortholog of mammalian ALDH1, and the identity of rat ALDH-PB is commonly inter
101 binding site than those of related mammalian ALDH1 enzymes with the cofactor bound in the "hydride tr
104 s displaying the stem/progenitor cell marker ALDH1 and a decrease in cells expressing luminal epithel
107 ative immunofluorescence was used to measure ALDH1 in 134 patients with NSCLC from Yale University an
109 ly, LDN193189 blocks reconstitution of mixed ALDH1(+)/ALDH1(-) cultures indicating that BMP signaling
115 provide a basis for testing the efficacy of ALDH1 gene transduction to protect bone marrow cells fro
121 TD cells are characterized by high levels of ALDH1 enzymatic activity, related to high-level expressi
123 further demonstrated with an E399Q mutant of ALDH1 whose rate-limiting step had been changed from NAD
124 t only gives a view of a "natural mutant" of ALDH1 illustrating the adaptive conflict that can arise
125 inical problems associated with mutations of ALDH1, ALDH2, ALDH4, ALDH10 and succinic semialdehyde (S
127 positively correlated with the percentage of ALDH1+ tumor cells; this was further validated in an ind
128 raftment was correlated with the presence of ALDH1-positive CSCs, which predicted prognosis in patien
129 and in vivo studies show that the progeny of ALDH1(+)/CD90(-)/Ecad(-) cells residing in the adult mou
132 Additionally, a significant reduction of ALDH1, CD44 and Oct-3/4, key markers of pancreatic CSC w
134 gen/ITGA1 signaling promotes the survival of ALDH1-positive stem-like cells and cooperates with TGFbe
135 that were also ALDH1(+), implying that only ALDH1(+) EMT cells had the ability to seed a new epithel
139 ests that elevated hepatic RA down-regulates ALDH1 in a unique feedback pathway to control RA biosynt
142 10(3), and 1 x 10(3) s-1 M-1 ALDH1-sulfone, ALDH1-sulfoxide, ALDH2-sulfone, and ALDH2-sulfoxide, res
145 ncer stem cell marker, but demonstrated that ALDH1 is associated with CD44 expression, chemoresistanc
146 e we describe the first direct evidence that ALDH1 plays a physiological role in retinoic acid synthe
148 atory and retrospective study indicates that ALDH1 expression is associated with favorable outcome.
152 hich the RARalpha and C/EBPbeta activate the ALDH1 gene promoter through the RARE and C/EBP response
154 ' and directly adjacent to the RARE, and the ALDH1 gene is down-regulated in C/EBPbeta-null mouse liv
155 also enhanced mammosphere formation and the ALDH1+ population in estrogen receptor-positive mammary
156 elf-renewal of ER-MC cells and increased the ALDH1+ population, whereas siRNA-mediated depletion of A
157 etermine the mechanism of suppression of the ALDH1 gene by RA, transactivation studies were carried o
161 ignificantly reduced cell proliferation, the ALDH1(+) and CD44(+)/CD24(-) CSC subpopulations, and mam
162 s diminished oncogenic activity, reduced the ALDH1-positive cell population, and increased reactive o
163 protein (C/EBPbeta) also transactivates the ALDH1 gene promoter through a CCAAT box located 3' and d
164 receptor alpha (RARalpha) transactivates the ALDH1 gene promoter through a complex with an RA respons
165 cell organization of breast cancer with the ALDH1-positive CSCs constituting the tumorigenic cell po
166 group had shorter survival compared with the ALDH1-positive group in the Yale cohort (P = 0.00001), b
167 in indicates that diversification within the ALDH1/2/5/6 gene cluster occurred during the Neoproteroz
168 rozygosity for BRCA1 was documented in these ALDH1-positive lobules but not in adjacent ALDH1-negativ
170 nfer tumor-initiating properties in non-TICs/ALDH1(-)CD44(-)-HNC and this effect could be abrogated b
171 ression or ADAM17 overexpression in non-TICs/ALDH1(-)CD44(-)-HNC cells increased expression and secre
172 medium from Spg-miR145-transfected non-TICs/ALDH1(-)CD44(-)-HNC cells was sufficient to confer tumor
177 tumor cell lines in vitro, we tested whether ALDH1 overexpression could directly induce cyclophospham
183 h mRNAs encoding the mouse, chick or Xenopus ALDH1 homologs induced high levels of retinoic acid dete
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