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 expression significantly promotes tumor initiation

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

23 Among ALDHs, the rat ALDH1A7 gene displays a curious strain de

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

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

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

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

28 (w) cells) and human (CD34(+), CD133(+), and ALDH(hi) cells) HSC self-renewal ex vivo.

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

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

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

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

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

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

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

36 suppresses sarcosphere formation, as well as ALDH activity.

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

38 ce, and then overviews the various available ALDH inhibitors with a focus on the clinical potential a

39 bona fide enzyme, exhibiting NAD(+)-binding, ALDH activity, and esterase activity.

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

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

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

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

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

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

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

47 ot the stiff cells, isolated from CD133(+) , ALDH(+) , or side population CSCs, are able to form a tu

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

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

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

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

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

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

54 t with enrichment for stem/progenitor cells, ALDH+ cells have greater WNT signaling.

55 rnary structural interactions of the classic ALDH superfamily dimer, a phenomenon we call "trans-hier

56 dimer in solution, which mimics the classic ALDH superfamily dimer-of-dimer tetramer.

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

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

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

60 Combining ALDH inhibition with other kinase-directed treatments de

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 nt increased MFE and aldehyde dehydrogenase (ALDH) activity of patient-derived xenograft (PDX) tumors

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

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

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

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

83 and increases their aldehyde dehydrogenase (ALDH) activity, which was identified to be the key mecha

84 gated based on their aldehyde dehydrogenase (ALDH) activity.

85 cture shows that the aldehyde dehydrogenase (ALDH) and alcohol dehydrogenase (ADH) active sites resid

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

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

88 The aldehyde dehydrogenase (ALDH) family of metabolic enzymes converts aldehydes to

89 logs represent a new aldehyde dehydrogenase (ALDH) family with different substrate preferences from r

90 ta plants possess an aldehyde dehydrogenase (ALDH) gene named ALDH12.

91 p53 and aldehyde dehydrogenase (ALDH) have been implicated in key tumorigenesis processe

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

93 The aldehyde dehydrogenase (ALDH) superfamily is a vast group of enzymes that cataly

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

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

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

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

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

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

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

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

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

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

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

105 ke associated enzyme aldehyde dehydrogenase (ALDH).

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

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

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

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

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

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

112 Aldehyde dehydrogenases (ALDHs) are highly expressed in the chemotherapy- and rad

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

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

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

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

117 cription factor for aldehyde dehydrogenases (ALDHs).

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

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

120 ehaviors of the hydrolytic and CoA-dependent ALDHs.

121 hanisms and evolution of NAD(P)(+)-dependent ALDHs.

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

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

124 ammatory signaling in distal differentiated (ALDH-) TE.

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

126 uman ovarian tumors and cell lines displayed ALDH activity.

127 On the contrary, lung metastasis displayed ALDH+/CD133+ and MET-like phenotype with oxidative metab

128 al TE cell populations finds that the distal ALDH+ TE cells exhibit pronounced expression of gene set

129 nctional states are associated with distinct ALDH isoform transcriptomic signatures.

130 Knockdown of the dominant ALDH isoform in high AVS HNSCC depleted the CIC pool in

131 ed structure-activity relationships for each ALDH isoenzyme.

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

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

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

135 d with salisphere assays, flow cytometry for ALDH/CD44 (CSC markers for MEC), and Western blots for B

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

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

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

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

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

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

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

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

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

149 s showed that HPV16+/p53WT cases have higher ALDH variance score (AVS), a measure of tumor ALDH isofo

150 stem cells that exhibited relatively higher ALDH activity.

151 presentation in 13 Pfam terms including HSP, ALDH and ubiquitin families in Dalbergia.

152 Aldehyde hydrogenases (ALDHs) belong to a large gene family involved in oxidati

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

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

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

156 BKM120 induced higher levels of apoptosis in ALDH(+) or CD44(+)/CD24(-) populations, respectively, th

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

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

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

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

161 m-tolerant cells and tumors were enriched in ALDH(+) cells, formed more spheroids, and expressed incr

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

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

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

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

166 1 expression is associated with increases in ALDH activity and is detectable in stem-like cells when

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

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

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

170 -23b decreased LGR5 expression and increased ALDH(+) CSCs.

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

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

173 AVS and several individual ALDH isoforms were associated with prognosis in HPV16+/p

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

175 butylthiocarbamate sulfoxide, which inhibits ALDH at nanomolar levels.

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

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

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

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

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

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

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

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

184 4Luc2 PCa cells compared with non-metastatic ALDH(low).

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

186 tification and development of small molecule ALDH inhibitors.

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

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

189 However, inhibiting multiple ALDH family members can be toxic and isoform-specific in

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 Analysis of ALDH+ cells from endocrine-resistant patient samples rev

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 We found that PDAC consists of ALDH+/CD133+ and drug-resistant (MDR1+) subtypes of CSCs

197 Accordingly, the development of ALDH inhibitors may be the most direct approach to targe

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

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

200 micking environment showed the enrichment of ALDH+/CD133+ populations.

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

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

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 al compared with patients with low levels of ALDH.

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

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

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

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

213 both IL6 and LIF increased the percentage of ALDH+ ovarian cancer stem-like cells (CSC).

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

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

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

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

218 This review discusses the role of ALDH in cancer and therapy resistance, and then overview

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

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

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

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

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

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

225 t substrate preferences of VvAHGD from other ALDHs.

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

227 3 in aldehyde dehydrogenase (ALDH)-positive (ALDH(+)) and CD133-positive (CD133(+)) subpopulations of

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

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

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

231 ied as ALDH4), which are the closest related ALDH superfamily members.

232 ifferent substrate preferences from reported ALDH families, named the L-AHGDH family.

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

234 determine the percentages of drug-resistant ALDH+ cells, MDR-1/ABCG2 overexpressing cells, and cance

235 interested in developing novel and selective ALDH inhibitors.

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

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

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

239 , our novel findings on the role of the SOX9-ALDH axis support the use of this CSC regulator as a pro

240 unified nomenclature for the entire soybean ALDH gene families.

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

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

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

244 In this study, ALDH isoform expression diversity was revealed in CICs w

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

246 re research directions to effectively target ALDH in the management of cancer therapy resistance are

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

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

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

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

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

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

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

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

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 KM120 treatment simultaneously decreased the ALDH(+) and CD44(+)/CD24(-) TICs.

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

263 mixture (DSF/Cu) specifically decreased the ALDH(+) TIC population and treatment with BKM120, a pan-

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

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

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

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

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 nts led to a significant accumulation of the ALDH(+) TIC population.

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

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

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

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

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

276 ased architecture highly conserved along the ALDHs family.

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 Moreover, tumor ALDH profiling may provide insight on which ALDH isoform

283 LDH variance score (AVS), a measure of tumor ALDH isoform expression diversity, compared to HPV-/p53H

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

285 Using ALDH in combination with CD133 to analyze ovarian cancer

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

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

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

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

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

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

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

293 ALDH profiling may provide insight on which ALDH isoform to target in high AVS HNSCC tumors to deple

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