ライフサイエンスコーパス: ALDH

1 ALDH activity appears to distinguish normal from leukemi

2 ALDH activity is not only a marker for CSCs but also imp

3 ALDH can also identify stem cells in normal adult tissue

4 ALDH expression significantly promotes tumor initiation

5 ALDH(+) cells isolated from ovarian cancer cell lines we

6 ALDH(+) CSC from patients (n = 6) engrafted in hESCT wit

7 ALDH(+)/CD49f(+)/EpCAM(+) tumor and normal cells cluster

8 ALDH(-) ovarian cancer cells showed no engraftment in th

9 ALDH(br) (r = 0.78; 95% confidence interval [CI], 0.76-0

10 ALDH(hi) cells also exhibited greater clonogenic and org

11 ALDH(hi) cells transiently recruited to ischemic regions

12 ALDH(hi)Lin(-) cells were efficiently engrafted in the r

13 Notably, as few as 1,000 ALDH(+) cells isolated directly from CD133(-) human ovar

14 rs in immunocompromised mice, whereas 50,000 ALDH(-) cells were unable to initiate tumors.

15 Using the structure of a sheep class 1 ALDH, it was possible to deduce that the interaction bet

16 Strikingly, as few as 11 ALDH(+)CD133(+) cells isolated directly from human tumor

17 Aldehyde dehydrogenase 2 (ALDH2), one of 19 ALDH superfamily members, catalyzes the NAD(+)-dependent

18 w that a selective aldehyde dehydrogenase-2 (ALDH-2) inhibitor, ALDH2i, suppresses cocaine self-admin

19 CNDT2.5 ALDH+ cells formed spheres, whereas ALDH- cells did not.

20 sion of aldehyde dehydrogenase 1 isoform A3 (ALDH(+)) as beta cells become dedifferentiated.

21 pothesized that high level of ALDH activity (ALDH(hi)) in a tumor might positively correlate with the

22 population with intermediate ALDH activity (ALDH(int)) that contains leukemia stem cells (LSCs).

23 s with high aldehyde dehydrogenase activity (ALDH(hi)Lin(-)) into irradiated NOD/SCID/MPSVII mice fol

24 ing of most of the substrate classes of ADH, ALDH, and CYP.

25 The ADH-ALDH pathway also governs the metabolism of retinol (vit

26 In this study, we defined that the ADH-ALDH pathway serves as a potent antiviral host factor in

27 attenuates the antiviral function of the ADH-ALDH pathway, which suggests the possibility that EtOH-r

28 rospectively examined the correlations among ALDH(br), CD34(+), and CFU content of 3908 segments over

29 This mode of regulation of an ALDH has not been described before.

30 Glycolytic activity and ALDH activity were significantly elevated in Mes GSCs bu

31 heir radioresistant derivatives, ALDH(+) and ALDH(-) cell populations revealed the mechanisms, which

32 we report that dual positivity of CD133 and ALDH defines a compelling marker set in ovarian CSC.

33 ted to small intestine epithelial cells, and ALDH activity in CRBPII(-/-) DCs was restored by transfe

34 mentin expressions, higher clonogenicity and ALDH positive expression of cancer cells cultured in a d

35 cant, positive association between EPHA2 and ALDH expression, indicating an important role for EPHA2

36 or cell migration, tumorsphere formation and ALDH-positive cancer stem cell population, in vitro.

37 D1, and the stem-cell related genes KLF4 and ALDH in BT474 cells.

38 that distinct subpopulations of LGR5(+) and ALDH(+) CSCs exist.

39 hich a pharmacologic agent recruited another ALDH to metabolize acetaldehyde.

40 suppresses sarcosphere formation, as well as ALDH activity.

41 ongly correlated with CFU content as well as ALDH(br) content of the CBU.

42 BM ALDH(hi) cells were enriched for myelo-erythroid progeni

43 Thus, human BM ALDH(hi) cells represent a progenitor-enriched populatio

44 shed the tumor-initiating properties of both ALDH(+) and CD29(hi)CD61(+) BCSC, as achieved by impairi

45 d to define the relationship of ALDH-bright (ALDH(br)) cells with previously defined EPCs, patient ag

46 enzyme aldehyde dehydrogenase (ALDH bright [ALDH(br)]), along with viable CD45(+) or CD34(+) cell co

47 ncer stem-like cells (BCSC) as identified by ALDH(+) and CD29(hi)CD61(+) markers, respectively, in mu

48 f NO and cGMP accumulation were inhibited by ALDH inhibitors chloral hydrate and daidzin.

49 ow that vitamin A metabolism, as measured by ALDH activity, was preferentially found in CD103(+)CD11b

50 reduced IL-6 production from CD103(+)CD11b(+)ALDH(-) colonic DCs in Aoah(-/-) mice compared with Aoah

51 ntified a colonic DC subset (CD103(+)CD11b(+)ALDH(-)) displaying a unique capacity to both express AO

52 of CIC-associated markers (e.g., CD44, CD24, ALDH-1, EpCAM, Lgr5), multipotency, and tumorigenicity f

53 Clonal CD27(+)ALDH(high) B cells, sharing immunoglobulin gene rearrang

54 remission was enriched for the CD34(+)CD38(-)ALDH(int) leukemic cells, and the presence of these cell

55 ytoskeleton remodeling, with CD24(-)/CD44(+)/ALDH(+) stem cell populations present exhibiting a highe

56 smaller fraction of cancer stem-like cells (ALDH(+)CD44(+)) and were less invasive than tumors vascu

57 ) mice, whereas 10,000 noncancer stem cells (ALDH-CD44-Lin-) resulted in 2 tumors in 15 mice.

58 of highly metastatic and tumorigenic cells (ALDH(high)) strongly affected the invasive cytoskeleton,

59 The Rossmann domain resembles the classic ALDH superfamily NAD(+)-binding domain, whereas the flap

60 ed as undifferentiated and highly clonogenic ALDH(+)/CD49f(+)/EpCAM(+) luminal progenitors, which exp

61 ny primary cell lines failed to grow, CNDT96 ALDH+ cells formed spheres in anchorage-independent cond

62 Combining ALDH inhibition with other kinase-directed treatments de

63 intain serum retinol, was required to confer ALDH activity to CD103(+) LP DCs.

64 or dietary retinoids were required to confer ALDH activity to LP DCs in vivo.

65 Implantation of 1,000 CSC (ALDH+CD44+Lin-) led to tumors in 13 (out of 15) mice, wh

66 Compared with non-CSCs, ALDH+ cells demonstrated increased expression of activat

67 mall intestine epithelium and LP CD103(+) DC ALDH activity, and the ability to promote IgA production

68 Taken together, our findings define ALDH and CD133 as a functionally significant set of mark

69 levels of the enzyme aldehyde dehydrogenase (ALDH bright [ALDH(br)]), along with viable CD45(+) or CD

70 r cells positive for aldehyde dehydrogenase (ALDH(+)) had increased ability to form mammospheres comp

71 lls purified by high aldehyde dehydrogenase (ALDH(hi)) activity, a progenitor cell function conserved

72 we demonstrated that aldehyde dehydrogenase (ALDH) 1a1 is the major ALDH expressed in mouse liver and

73 by quantitating both aldehyde dehydrogenase (ALDH) activities and 5 signaling proteins in single MDA-

74 sphere formation and aldehyde dehydrogenase (ALDH) activity (Aldefluor) assays.

75 tyrosinase, enhanced aldehyde dehydrogenase (ALDH) activity and upregulation of histone demethylases.

76 istics, such as high aldehyde dehydrogenase (ALDH) activity due to ALDH1A1 expression, contributes to

77 f cells positive for aldehyde dehydrogenase (ALDH) activity from a green-fluorescent background is di

78 High levels of aldehyde dehydrogenase (ALDH) activity have been proposed to be a common feature

79 High aldehyde dehydrogenase (ALDH) activity is a marker commonly used to isolate stem

80 Aldehyde dehydrogenase (ALDH) activity is a reported CSC marker in several solid

81 study, we show that aldehyde dehydrogenase (ALDH) activity is indicative of radioresistant prostate

82 iate (int) levels of aldehyde dehydrogenase (ALDH) activity reliably distinguished leukemic CD34(+)CD

83 ration, chemodrug or aldehyde dehydrogenase (ALDH) activity selection.

84 ood,Gerber et al use aldehyde dehydrogenase (ALDH) activity to further subdivide the CD34(+)CD38(-) c

85 noma cells with high aldehyde dehydrogenase (ALDH) activity were enriched 16.8-fold in tumorigenic ce

86 on strategy based on aldehyde dehydrogenase (ALDH) activity, a common feature shared by many progenit

87 (EPC) assay based on aldehyde dehydrogenase (ALDH) activity, and to define the relationship of ALDH-b

88 n of the CSC markers aldehyde dehydrogenase (ALDH) and CD133.

89 of stem cell marker aldehyde dehydrogenase (ALDH) as well as by generation of hyperplastic lesions i

90 pathway, comprising aldehyde dehydrogenase (ALDH) family genes and in particular ALDH1A3, were enric

91 ydrogenase (ADH) and aldehyde dehydrogenase (ALDH) genes and alcohol dependence (AD) have long been s

92 Aldehyde dehydrogenase (ALDH) is a candidate marker for lung cancer cells with s

93 Aldehyde dehydrogenase (ALDH) overexpression is characteristic for both hematopo

94 ydrogenase (ADH) and aldehyde dehydrogenase (ALDH) play central roles.

95 The aldehyde dehydrogenase (ALDH) superfamily member Delta(1)-pyrroline-5-carboxylat

96 essed high levels of aldehyde dehydrogenase (ALDH), a detoxifying enzyme characteristic of many proge

97 l cells positive for aldehyde dehydrogenase (ALDH), a putative marker of precursor colon CSC (pCCSC).

98 RY-X cells expressed aldehyde dehydrogenase (ALDH), a stem cell marker.

99 Markers such as aldehyde dehydrogenase (ALDH), CD133, and CD44 have been successfully used to id

100 dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), flavin-containing monooxygenase (FMO), and cytoch

101 y immunostaining for aldehyde dehydrogenase (ALDH), keratocan, and CD34 and by the expression of kera

102 metabolite, inhibits aldehyde dehydrogenase (ALDH), leading to accumulation of the reactive dopamine

103 identified with anti-aldehyde dehydrogenase (ALDH)-1 and alpha-smooth muscle actin (alpha-SMA) antibo

104 aracterized STAT3 in aldehyde dehydrogenase (ALDH)-positive (ALDH(+)) and CD133-positive (CD133(+)) s

105 pathway reduces the aldehyde dehydrogenase (ALDH)-positive population in ERBB2-positive breast cance

106 and the expansion of aldehyde dehydrogenase (ALDH)-positive population, suggest that PHLDA1 may play

107 cer stem-like marker aldehyde dehydrogenase (ALDH).

108 ke associated enzyme aldehyde dehydrogenase (ALDH).

109 the stem cell marker aldehyde dehydrogenase (ALDH).

110 a RCC cell line, but aldehyde dehydrogenase (ALDH)1 and ALDH7 had no effect.

111 tion and activity of aldehyde dehydrogenase (ALDH)2, an enzyme that detoxifies reactive oxygen specie

112 cellular enzyme retinaldehyde dehydrogenase (ALDH) provides resistance to several toxic agents.

113 Aldehyde dehydrogenases (ALDH) catalyze the irreversible oxidation of aldehydes t

114 Aldehyde dehydrogenases (ALDH) participate in multiple metabolic pathways and hav

115 rboxyphosphamide by aldehyde dehydrogenases (ALDH), especially ALDH1A1 and ALDH3A1.

116 ic NAD(P)-dependent aldehyde dehydrogenases (ALDH).

117 Aldehyde dehydrogenases (ALDHs) are members of NAD(P)(+)-dependent protein superf

118 Aldehyde dehydrogenases (ALDHs) catalyze the NAD(P)(+)-dependent oxidation of ald

119 Human aldehyde dehydrogenases (ALDHs) comprise a family of 17 homologous enzymes that m

120 Aldehyde dehydrogenases (ALDHs) metabolize reactive aldehydes and possess importa

121 cription factor for aldehyde dehydrogenases (ALDHs).

122 e first crystal structure of a CoA-dependent ALDH.

123 the diet) and of cytosolic NAD(+)-dependent ALDH activity.

124 ehaviors of the hydrolytic and CoA-dependent ALDHs.

125 cer cells, their radioresistant derivatives, ALDH(+) and ALDH(-) cell populations revealed the mechan

126 de the basis for rational approach to design ALDH isoenzyme-specific inhibitors as research tools and

127 reas depletion of PDK1 remarkably diminishes ALDH(+) subpopulations, decreases stemness-related trans

128 uman ovarian tumors and cell lines displayed ALDH activity.

129 ed structure-activity relationships for each ALDH isoenzyme.

130 ive phosphorylated form of STAT3 than either ALDH(-)/CD133(-) or unfractionated colon cancer cells.

131 ntain a subpopulation of cells with elevated ALDH activity, and that this activity is associated with

132 ique ALDH sequences encoding members of five ALDH families involved in a wide range of metabolic and

133 ligomeric state is known to be important for ALDH function, the oligomerization of P5CDH has remained

134 may provide a suitable microenvironment for ALDH(high) prostate cancer cells to establish metastatic

135 port a red-shifted fluorescent substrate for ALDH, AldeRed 588-A, for labelling viable ALDH(pos) cell

136 yphenylacetaldehyde (DOPAL), a substrate for ALDH-2.

137 using Aldefluor, a fluorogenic substrate for ALDH.

138 significantly inhibited spheroid formation, ALDH expression and activity, chemoresistance, and tumor

139 LDH(+)CD133(+) cells could generate all four ALDH(+/-)CD133(+/-) cell populations and identified a cl

140 for multicolour applications to fractionate ALDH(pos) cells in the presence of green fluorophores in

141 Xenograft melanomas that developed from ALDH(+) cells displayed robust self-renewal, whereas tho

142 ayed robust self-renewal, whereas those from ALDH(-) cells showed minimal self-renewal in vitro.

143 To date, there are relatively few general ALDH inhibitors that can be used to probe the contributi

144 hich is the first observation of a hexameric ALDH in solution.

145 High ALDH activity is a feature of LPCs that can be taken adv

146 motherapy-resistant cells identified by high ALDH activity.

147 em cells have all been reported to have high ALDH activity, detected using Aldefluor, a fluorogenic s

148 ward hepatocyte-like cells of LPCs with high ALDH activity is also successfully applicable to human l

149 catenin signaling can further demarcate high-ALDH tumor-initiating cells in the nondysplastic epithel

150 stem cells that exhibited relatively higher ALDH activity.

151 The regenerative capacity of human ALDH(hi) cells was assessed by intravenous transplantati

152 contrast to what is observed for hydrolytic ALDHs, the nicotinamide ring is well defined in the elec

153 is possible in MSDH, as shown for hydrolytic ALDHs.

154 In support of this hypothesis, ALDH could be used to enrich for CSC in endometrial canc

155 own-regulated in mammospheres, as well as in ALDH(+) breast cancer cells.

156 LGR5 and miR-23b are inversely correlated in ALDH(+) CSCs and that distinct subpopulations of LGR5(+)

157 sting a further enrichment of ovarian CSC in ALDH(+)CD133(+) cells.

158 NOTCH3 resulted in a significant decrease in ALDH(+) lung cancer cells, commensurate with a reduction

159 tion of the WNT pathway led to a decrease in ALDH(+) tumor progenitor population and to radiosensitiz

160 tein 2 (BMP2) is preferentially expressed in ALDH(-)CD133(-) cells.

161 vated Notch pathway transcript expression in ALDH(+) cells.

162 ts and signal transducers CD126 and GP130 in ALDH(hi) endometrial cancer cells.

163 Notch activation, leading to an increase in ALDH high(+) cells.

164 1 expression is associated with increases in ALDH activity and is detectable in stem-like cells when

165 which GW9662 treatment causes a reduction in ALDH-positive population cells is partially due to ROS,

166 supporting a critical role for EGFL6/SHP2 in ALDH(+) cell maintenance.

167 Increased ALDH (e.g., ALDH1A1) gene expression and catalytic activ

168 -23b decreased LGR5 expression and increased ALDH(+) CSCs.

169 n cancer cells subpopulations show increased ALDH activity, higher ability to exclude Hoechst 33342,

170 ress diseases such as cancer where increased ALDH activity is associated with a cellular phenotype.

171 primary mesencephalic neurons (ii) inhibits ALDH and (iii) alters dopamine homeostasis.

172 butylthiocarbamate sulfoxide, which inhibits ALDH at nanomolar levels.

173 ty and the size of the metastasis-initiating ALDH(high) sub-population.

174 entify a unique population with intermediate ALDH activity (ALDH(int)) that contains leukemia stem ce

175 Isolated ALDH(+) lung cancer cells were observed to be highly tum

176 mistry and qPCR analyses on freshly isolated ALDH(+) cells reveal an enrichment in cells expressing l

177 ate that AldeRed 588-A successfully isolates ALDH(hi) human haematopoietic stem cells from heterogene

178 Cyclin A1 overexpression in the stem-like ALDH(high) subpopulation of PC3M cells, one model of pro

179 dehyde dehydrogenase (ALDH) 1a1 is the major ALDH expressed in mouse liver and is an effective cataly

180 eviously established cancer stem cell marker ALDH (aldehyde dehydrogenase) in the maintenance of this

181 eres and downregulated the stem cell markers ALDH and CD44, while upregulating CD24.

182 4Luc2 PCa cells compared with non-metastatic ALDH(low).

183 and display higher levels in the metastatic ALDH(high) sub-population of PC-3M-Pro4Luc2 PCa cells co

184 was transformed into a yeast strain missing ALDHs.

185 tification and development of small molecule ALDH inhibitors.

186 ntaining the equivalent of 2- to 4-fold more ALDH(hi) cells, mice transplanted with purified ALDH(hi)

187 Moreover, ALDH(+) MCL cells were relatively quiescent and resistan

188 Moreover, ALDH(high) tumor cells expressing elevated levels of aro

189 cancer cells based on enzymatic activity of ALDH (Aldefluor assay) and implantation of these cells i

190 IgG1 reduced the expression and activity of ALDH and correspondingly reduced both primary and second

191 nd inhibited the high glycolytic activity of ALDH(high) CSC to limit their self-renewal capability.

192 PAM50 gene-set analyses of ALDH(+)/CD49f(+)/EpCAM(+) populations efficiently identi

193 ion among EPC assays, and the association of ALDH(br) numbers with age and disease severity.

194 y the increased tumor-initiating capacity of ALDH(hi) cells in immunodeficient mice.

195 e report the discovery of a general class of ALDH inhibitors with a common mechanism of action.

196 The correlation of ALDH(br) cells with clinical factors and outcomes warran

197 these cells, and pharmacologic disruption of ALDH activity leads to accumulation of ROS to toxic leve

198 ted the migration and asymmetric division of ALDH(+) ovarian CSC.

199 wnregulation also decreased the frequency of ALDH(high) cells, impairing their tumor-initiating poten

200 pathway, and (ii) promotes the induction of ALDH activity in breast cancer cells.

201 HSCs, suggesting directly that inhibition of ALDH promotes HSC self-renewal via reduction of retinoic

202 eroline (THP) formation due to inhibition of ALDH-2 decrease cocaine-stimulated dopamine production a

203 Inhibition of ALDH-2 enables DOPAL to condense with dopamine to form T

204 Selective inhibition of ALDH-2 may have therapeutic potential for treating human

205 However, clinically applicable inhibitors of ALDH activity have not been reported.

206 C marker, we hypothesized that high level of ALDH activity (ALDH(hi)) in a tumor might positively cor

207 al mouse liver cells displays high levels of ALDH activity, allowing the isolation of these cells by

208 Progenitor cells display high levels of ALDH activity.

209 al compared with patients with low levels of ALDH.

210 Modulation of ALDH activity and retinoid signaling is a previously unr

211 d in the identification of a large number of ALDH genes, most of which still need to be functionally

212 Notably, the number of ALDH(hi) cells in tumor cell lines and primary tumors in

213 ilencing of EGFL6 or SHP2 limited numbers of ALDH(+) cells and reduced tumor growth, supporting a cri

214 eting LGR5, contributes to overpopulation of ALDH(+) CSCs and colorectal cancer.

215 ession in MCL and found small populations of ALDH(+) cells that were highly clonogenic.

216 Finally, the presence of ALDH(+)CD133(+) cells in debulked primary tumor specimen

217 nsion while suppressing the proliferation of ALDH(-)CD133(-) cells.

218 SGI-110 reduced the stem-like properties of ALDH(+) cells, including their tumor-initiating capacity

219 activity, and to define the relationship of ALDH-bright (ALDH(br)) cells with previously defined EPC

220 anti-Src short interfering RNA treatment of ALDH+ tumors reduced tumor mass by 91%.

221 The level of ALDHs enzymatic activity has been used as a cancer stem

222 ar metabolic pathways of selected members of ALDHs in soybean responses to environmental stress condi

223 usly determined the numbers of EPCs based on ALDH activity and cell surface expression of CD133, CD34

224 An assay based on ALDH activity may offer a simple means for enumerating E

225 the intrabursal model, but had no effect on ALDH.

226 We found that only ALDH(+)CD133(+) cells could generate all four ALDH(+/-)C

227 ve for human ALDH1A1 compared to eight other ALDH isoenzymes.

228 noma cells have enhanced tumorigenicity over ALDH(-) cells and superior self-renewal ability.

229 3 in aldehyde dehydrogenase (ALDH)-positive (ALDH(+)) and CD133-positive (CD133(+)) subpopulations of

230 luor assay, aldehyde dehydrogenase-positive (ALDH+) cells comprised 5.8% +/- 1.4% (mean +/- standard

231 BMP2 promotes ALDH(+)CD133(+) cell expansion while suppressing the pro

232 H(hi) cells, mice transplanted with purified ALDH(hi) cells showed augmented recovery of perfusion an

233 006 (CpG) reduced the frequency of quiescent ALDH(+) MCL cells, induced terminal plasma cell differen

234 m cells; cyclopamine preferentially reduced "ALDH-high" cells by approximately 3-fold (P = 0.048).

235 arian tumor cells and vasculature, regulates ALDH(+) ovarian CSC.

236 that CpG may target clonogenic and resistant ALDH(+) cells as well as improve the activity of proteas

237 interested in developing novel and selective ALDH inhibitors.

238 H superfamily fold is well established, some ALDHs contain an uncharacterized domain of unknown funct

239 Flow-sorted ALDH(+) islet cells demonstrate impaired glucose-induced

240 Depletion of EPHA2 in sorted ALDH(+) populations markedly inhibited tumorigenicity in

241 unified nomenclature for the entire soybean ALDH gene families.

242 AldeRed 588-A stains ALDH(pos) murine pancreatic centroacinar and terminal du

243 We studied ALDH expression in MCL and found small populations of AL

244 a useful tool to select stem cells or study ALDH within a green-fluorescent background.

245 and extraterminal (BET) inhibitors suppress ALDH activity by abrogating BRD4-mediated ALDH1A1 expres

246 s JQ1, is a promising strategy for targeting ALDH activity in epithelial ovarian cancer.

247 ed more potent tumor-initiating ability than ALDH(-)/CD133(-) cells in tumor xenograft assays in mice

248 rated more tumors, with shorter latency than ALDH- or sham-sorted cells.

249 These data demonstrated that ALDH and CD44 select a subpopulation of cells that are h

250 We demonstrated that ALDH(+) ovarian cancer cells possess multiple stem cell

251 RNA sequencing analysis demonstrates that ALDH(+) cells are characterized by: (i) impaired oxidati

252 We find that ALDH protects the drug-tolerant subpopulation from the p

253 We found that ALDH(+)/CD133(+) cells expressed higher levels of the ac

254 Taken together, these findings indicate that ALDH selects for a subpopulation of self-renewing NSCLC

255 Taken together, our results indicate that ALDH(+) cells contribute to tumor radioresistance and th

256 -renew was confirmed by the observation that ALDH+CD44+Lin- cells sorted from human HNSCC formed more

257 Research evidence has shown that ALDHs represent a promising class of genes to improve gr

258 Although the ALDH superfamily fold is well established, some ALDHs co

259 first structure of a protein containing the ALDH superfamily DUF.

260 In culture, the ALDH(+) population can give rise to functional hepatocyt

261 EPHA2 in multiple NSCLC lines decreased the ALDH(+) cancer stem-like population and tumor spheroid f

262 hile showing robust cell death, enriches the ALDH(+) stem-like cells through EGFR-dependent activatio

263 novel dimer that has never been seen in the ALDH superfamily.

264 ines, we observed even greater growth in the ALDH(+)CD133(+) cells compared with ALDH(+)CD133(-) cell

265 of breast carcinoma cell lines increases the ALDH-expressing 'cancer stem cell' population which disp

266 In the NSG mouse, the ALDH expressing cell population was enriched 100-fold in

267 Compared to other members of the ALDH family, FDH demonstrates a new mode of binding of t

268 RelB also affected expression of the ALDH gene ALDH1A2 Interestingly, classical NFkappaB sign

269 In this paper, we identify members of the ALDH gene superfamily in soybean genome, and provide a u

270 n cancer cells and increases the size of the ALDH(high) sub-population.

271 Only the ALDH(+) cells were capable of secondary spheroidgenesis,

272 These results suggest that the ALDH(br) segment assay (based on unit characteristics me

273 e dehydrogenase site and NAD(+) bound to the ALDH site were determined in two space groups at 1.7-1.9

274 hereas the flap is strikingly similar to the ALDH superfamily dimerization domain.

275 ased architecture highly conserved along the ALDHs family.

276 capable of self-renewal compared with their ALDH(-) counterparts.

277 This ALDH model for PD etiology may help explain the selectiv

278 targeting of the Notch pathway reduces this ALDH(+) component, implicating Notch signaling in lung c

279 Thus, ALDH(+) melanoma cells have enhanced tumorigenicity over

280 sed ability to form mammospheres compared to ALDH(-) cells.

281 downregulated proteins such as DPYSL2, TPI1, ALDH, and UCHL1 were found to play critical roles in the

282 o ischemic tissue, suggesting that transient ALDH(hi) cell engraftment stimulated endogenous revascul

283 The soybean genome contains 18 unique ALDH sequences encoding members of five ALDH families in

284 Using ALDH in combination with CD133 to analyze ovarian cancer

285 lls that can be prospectively enriched using ALDH(+)CD44(+)alpha2beta1(+) phenotype.

286 ors, compared with ALDH(-) cells, validating ALDH as a marker of ovarian CSC in cell lines.

287 or ALDH, AldeRed 588-A, for labelling viable ALDH(pos) cells.

288 In vivo, ALDH+ CNDT2.5 cells generated more tumors, with shorter

289 in anchorage-independent conditions, whereas ALDH- cells did not.

290 mammary stem cell-associated genes, whereas ALDH(+) BCSC were more closely associated with luminal p

291 CNDT2.5 ALDH+ cells formed spheres, whereas ALDH- cells did not.

292 We sought to determine whether ALDH can be used as a marker to isolate tumor-initiating

293 also identify a molecular mechanism by which ALDH-2 inhibition reduces cocaine-seeking behavior: incr

294 We found that cells with ALDH activity are abundant in the mouse pancreas during

295 We further demonstrate that cells with ALDH activity can commit to either endocrine or acinar l

296 dy, we isolated and characterized cells with ALDH activity in the adult mouse or human pancreas durin

297 h in the ALDH(+)CD133(+) cells compared with ALDH(+)CD133(-) cells, suggesting a further enrichment o

298 nd preferentially grew tumors, compared with ALDH(-) cells, validating ALDH as a marker of ovarian CS

299 and organoid-forming capacity compared with ALDH(lo) cells.

300 With Intermittent Claudication Injected With ALDH Bright Cells) is a National Heart, Lung, and Blood