ライフサイエンスコーパス: diaphorase

1 lation with the cellular concentration of DT-diaphorase.

2 differential substrate specificities for DT-diaphorase.

3 potential cytotoxic prodrugs activated by DT-diaphorase.

4 ones and phenindone in the active site of DT-diaphorase.

5 poor substrates, some of which inactivate DT-diaphorase.

6 oreactive cells were also positive for NADPH-diaphorase.

7 nicotinamide adenine dinucleotide phosphate diaphorase.

8 y several bioreductive enzymes, including DT-diaphorase.

9 for human cancer chemotherapy mediated by DT-diaphorase.

10 llar vesicles in the presence of NADH and DT-diaphorase.

11 odose also were stained positively for NADPH-diaphorase.

12 ron carrier, whereas hydrogenase (1.1 U) and diaphorase (0.8 U) did not.

13 chrome b5 reductase 3 (CYB5R3, also known as diaphorase 1).

14 e (12.2 U), fumarate reductase (13.1 U), and diaphorase (109.7 U) activities.

15 lls with a plasmid containing 3 kb of the DT-diaphorase 5' region upstream of a reporter gene, chlora

16 study was to determine the changes in NADPH-diaphorase (a commonly used marker for neuronal NOS acti

17 immunoreactive neurons did not contain NADPH-diaphorase, a marker for nitric oxide synthase.

18 ed for dual localization of Phox2a and NADPH diaphorase, a marker of nitric oxide-containing neurons.

19 the development of neurons expressing NADPH-diaphorase activity (an early marker found in inhibitory

20 nicotinamide adenine dinucleotide phosphate-diaphorase activity (NADPHd) were quantified at 500 micr

21 NADPH-diaphorase activity also was observed in the lateral and

22 ilar to iNOSFL, iNOS8(-)9(-) exhibited NADPH-diaphorase activity and contained tightly bound calmodul

23 dy demonstrates the co-localisation of NADPH diaphorase activity and GFAP immunoreactivity in non-neu

24 hout this period, the optic lobes show NADPH-diaphorase activity and stain with an antibody to nitric

25 s contained little iNOS antigen and no NADPH diaphorase activity and were minimally able to convert L

26 was measured, and thus, may overestimate DT-diaphorase activity in cells having activity.

27 literature relating to the presence of NADPH-diaphorase activity in hippocampal principal cells.

28 to basal and injury-induced levels of NADPH diaphorase activity in MNs.

29 The intensity of NADPH-diaphorase activity in pyramidal cells located in the ve

30 vestigated the early postnatal expression of diaphorase activity in the hamster cochlea.

31 The diaphorase activity in the NADPH-cytochrome c reductase-

32 The rNoxA2 is an oxidase with diaphorase activity in the presence of electron acceptor

33 Tuberculosis patients' macrophages displayed diaphorase activity in the same proportion that they sta

34 ever, cytotoxicity did not correlate with DT-diaphorase activity in these cell lines.

35 these methods have been utilized to assay DT-diaphorase activity in tissue and cell homogenates.

36 If NADPH-diaphorase activity is an indicator of NOS, then our res

37 cal determinants of CA1 pyramidal cell NADPH-diaphorase activity is shown to be incubation of brains

38 and may account for the greater apparent DT-diaphorase activity measured with this compound.

39 In this report, the INT diaphorase activity of disrupted bovine polymorphonuclea

40 The diaphorase activity of NO synthase was used as a marker

41 Here, we show that: (i) neuronal NOS has PQ diaphorase activity that inversely correlates with NO fo

42 ce of menadione bisulfite, an artifactual DT-diaphorase activity was also detected, but was about one

43 When DT-diaphorase activity was measured as dicumarol-inhibitabl

44 The restrained-induced NADPH-diaphorase activity was significantly higher in the rost

45 ctions in ischemia-induced BH4 levels, NADPH-diaphorase activity, and caspase-3 gene expression in th

46 cyclic guanosine monophosphate (cGMP), NADPH diaphorase activity, and nitrotyrosine occurred 3 days a

47 sensitivity to MC by increasing levels of DT-diaphorase activity, properties not adequately explained

48 inea pig hearts stained positively for NADPH-diaphorase activity, suggesting that these cells do expr

49 ifferent tissues of tomato plants all showed diaphorase activity, with FNR II being more active than

50 e mutations also enhanced proteolytic and/or diaphorase activity.

51 amide adenine dinucleotide phosphate (NADPH) diaphorase activity.

52 (eNOS)--these cells also co-localised NADPH diaphorase activity.

53 so found to contain NOS and to possess NADPH-diaphorase activity.

54 glycosylase, whereas iNOS deficiency blocked diaphorase activity.

55 xylase, somatostatin, substance P, and NADPH diaphorase activity.

56 FNR), as were antibody reactivity to FNR and diaphorase activity.

57 LES-projecting neurons also contained NADPH-diaphorase activity; however, TH immunoreactivity was ne

58 reduction is catalyzed by the flavoprotein "diaphorase" activity of NOS.

59 An enzyme exhibiting NADH oxidase (diaphorase) activity was isolated from the hyperthermoph

60 The PBIs are reductively activated by DT-diaphorase and alkylate the phosphate backbone of DNA vi

61 he ventromedial nucleus contained both NADPH diaphorase and brain nitric oxide synthase as demonstrat

62 That NADPH diaphorase and brain nitric oxide synthase were found in

63 The interaction between DT-diaphorase and CoQ was also demonstrated in an isolated

64 cells was shown by co-localization of NADPH diaphorase and estrogen receptor and brain nitric oxide

65 amide adenine dinucleotide phosphate (NADPH)-diaphorase and Fos.

66 igh specificity for the activating enzyme DT-diaphorase and high percent DNA alkylation.

67 chondria in mSOD1 mouse MNs accumulate NADPH diaphorase and inducible nitric oxide synthase (iNOS)-li

68 ere modeled into the active site of human DT-diaphorase and minimized.

69 were extremely rich in VIP, nNOS, and NADPH-diaphorase and moderate in CHAT.

70 The overexpression of DT-diaphorase and NADPH:cytochrome c (P-450) reductase, two

71 The distribution of the enzymes NADPH diaphorase and nitric oxide synthase in the ventromedial

72 fter injury, and these cells exhibited NAPDH diaphorase and NOS activity.

73 es were also demonstrated in SM, using NADPH-diaphorase and NOS immunoreactivity, indicating nitroxid

74 sorcinol analogues is independent of NQO1/DT-diaphorase and P-glycoprotein expression.

75 her NOS might alternatively function as a PQ diaphorase and reexamined the question of whether NO/O-(

76 r revealed that DLD could also function as a diaphorase and serine protease.

77 to design poor to excellent substrates of DT-diaphorase and take advantage of varying levels of this

78 These data indicate that NOS is a PQ diaphorase and that toxicity of such redox-active compou

79 bstrate specificity for human recombinant DT-diaphorase and the cytotoxicity in the human H460 non-sm

80 icotinamide adenine dinucleotide phosphotase diaphorase, and arginine vasotocin were used in the pres

81 n C treatment results in the induction of DT-diaphorase as reflected in elevated steady state DT-diap

82 erhaps due to the lack of inactivation by DT-diaphorase as well as topoisomerase II inhibition.

83 mary assay and no activity in the counter DT-diaphorase assay.

84 or gamma-GCS, and a peak of 4.14-fold for DT-diaphorase at 250 mg/m2 ; higher doses were not more eff

85 ied human NAD(P)H:quinone oxidoreductase (DT-diaphorase), bioreductive activation to DNA-damaging spe

86 e compounds which are poor substrates for DT-diaphorase but have high hypoxic cytotoxicity ratios.

87 vessels exhibited strong staining for NADPH-diaphorase but no nNOS immunoreactivity.

88 Purified DT-diaphorase can be assayed as either dicumarol-inhibitabl

89 rom superoxide anion likely produced from DT-diaphorase catalysed reaction using oxygen as electron a

90 The two-electron bioreductive enzyme DT-diaphorase catalyzes the metabolism of quinones.

91 ntire ventromedial nucleus showed that NADPH diaphorase cellular staining was localized primarily in

92 This reaction is inhibited by addition of diaphorase, consistent with a radical mechanism for C-C

93 igh density of nNOS immunopositive and NADPH-diaphorase containing neurons and fibers at the rostral

94 Levels of gamma-GCS and DT-diaphorase correlated closely (P < or = 0.001) between p

95 The function of DT-diaphorase could be thus a major, if not the only, cause

96 lly generated NADPH is then amplified by the diaphorase cycling system to produce a highly fluorescen

97 ollowing: DT-diaphorase substrate design, DT-diaphorase-cytotoxicity quantitative structure-activity

98 er the soluble rat cytochrome b(5) reductase diaphorase domain to utilize NADPH as the preferred elec

99 etermined for the soluble, flavin-containing diaphorase domains of the rat and pig enzymes, no X-ray

100 nterest has been centered upon the enzyme DT-diaphorase (DTD) although conflicting reports of good an

101 none phosphoramidate prodrugs targeted to DT-diaphorase (DTD) have been synthesized and evaluated.

102 mycin C (MC) was reductively activated by DT-diaphorase [DTD; NAD(P)H:quinone oxidoreductase] from ra

103 DT-diaphorase (EC 1.6.99.2), also referred to as NAD(P)H:(q

104 NAD(P)H: quinone oxidoreductase-1 (NQO1, DT-diaphorase, EC 1.6.99.2).

105 eptor oxidoreductase (QR1, NQO1, formerly DT-diaphorase; EC ) protects animal cells from the deleteri

106 ntity to human NAD(P)H:quinone reductase (DT-diaphorase; EC 1.6.99.2), here designated QR1 and 82% id

107 Combined techniques for NADPH-diaphorase enzyme histochemistry and huntingtin immunocy

108 affecting principally parvalbumin- and NADPH diaphorase-expressing interneurons.

109 uences neuronal process projection for NADPH diaphorase-expressing, but not acetylcholinesterase-, ch

110 The onset of diaphorase expression in the spiral ganglion cells corre

111 As early as week 6 (W6) of gestation, diaphorase expression was observed in sympathetic pregan

112 s provide support for the hypothesis that DT-diaphorase functions as an antioxidant in both artificia

113 or alternative splicing in the control of DT-diaphorase gene expression.

114 elements in the 5' flanking region of the DT-diaphorase gene.

115 NADPH diaphorase histochemical and NOS I immunohistochemical s

116 etyltransferase immunocytochemical and NADPH diaphorase histochemical preparations at ages (postnatal

117 amide adenine dinucleotide phosphate (NADPH)-diaphorase histochemistry and in situ hybridization.

118 leus of the trapezoid body (MNTB) with NADPH-diaphorase histochemistry and in situ hybridization.

119 ith either ChAT immunocytochemistry or NADPH-diaphorase histochemistry and they appeared to be aligne

120 sed nicotinamide adenine diphosphate (NADPH)-diaphorase histochemistry as an indicator of nitric oxid

121 NADPH-diaphorase histochemistry has been shown to stain cells

122 ons and fibers were also identified by NADPH-diaphorase histochemistry in sections and whole-mount sp

123 We used a modified form of NADPH diaphorase histochemistry to compare the neuroanatomy of

124 amide adenine dinucleotide phosphate (NADPH)-diaphorase histochemistry to identify populations of neu

125 amide adenine dinucleotide phosphate (NADPH)-diaphorase histochemistry to investigate nitric oxide as

126 ult chinchilla and rat vestibular brainstem; diaphorase histochemistry was done in the chinchilla per

127 de synthase activity (visualized using NADPH-diaphorase histochemistry) was undetectable in the vicin

128 ainstem nuclei were also visualized by NADPH-diaphorase histochemistry, a marker of nNOS activity.

129 Using NADPH-diaphorase histochemistry, neuronal nitric oxide synthas

130 ergic (NANC) relaxation, NOS activity, NADPH diaphorase histochemistry, NOS immunohistochemistry, NOS

131 -nicotinamide adenine dinucleotide phosphate-diaphorase histochemistry.

132 amide adenine dinucleotide phosphate (NADPH)-diaphorase histochemistry.

133 nhibitors was investigated with wild-type DT-diaphorase (human and rat) and five mutants [three rat m

134 the k(cat) values for the wild-type human DT-diaphorase, hY155F, hH161Q, and hP187S were measured as

135 rations contained FSP27, ribophorin I, EHD2, diaphorase I, and ancient ubiquitous protein.

136 matic assays conducted in the presence of DT-diaphorase illustrate that the new probe shows reversibl

137 Furthermore, NADPH-diaphorase immunohistochemical staining of neurons in th

138 A functional homologue of DT-diaphorase in Giardia, NADH oxidase, uses oxygen as the

139 the most ideal prodrugs for activation by DT-diaphorase in human tumors.

140 e data demonstrate that the expression of DT-diaphorase in hyman cells is polymorphic, and that the l

141 ity (V(max)/K(M)) < 10 x 10(-4) s(-1) for DT-diaphorase in order not to be too toxic or nonselective.

142 e frequency of expression of this form of DT-diaphorase in the general population, we examined mRNA o

143 ally, the staining pattern of nNOS and NADPH-diaphorase in the NTS was similar.

144 imes more active than the human wild-type DT-diaphorase in the reduction of CB1954.

145 The localization of NADPH-diaphorase in these efferents indicated that they may us

146 f identified neurons were positive for NADPH-diaphorase in various central ganglia, including the met

147 utamylcysteine synthetase (gamma-GCS) and DT-diaphorase increased after dosing to reach a peak on day

148 tion of dicoumarol, a potent inhibitor of DT-diaphorase, interfered with the protection provided by C

149 e conclude that (i) fixative-resistant NADPH-diaphorase is a characteristic marker of 12-15% of neuro

150 Overexpressed DT-diaphorase is accompanied by increased intracellular hyd

151 NADPH diaphorase is also present in a subpopulation of type I

152 electron reduction to the hydroquinone by DT-diaphorase is known to deactivate these compounds.

153 Giardia NAD(P)H:menadione oxidoreductase (DT-diaphorase) is known to catalyse a single electron trans

154 , as defined mainly by the presence of NADPH diaphorase, is present in a subpopulation of both brains

155 e excellent substrates for purified human DT-diaphorase (k(cat)/K(m) = 3 x 10(7) - 3 x 10(8) M(-1) s(

156 In addition, two "U-shaped" groups of diaphorase-labeled cells were identified around the vent

157 than 400 microns was removed, no 'U-derived' diaphorase-labeled cells were present, whereas if only 2

158 nicotinamide adenine dinucleotide phosphate diaphorase localized NO synthase activity to MPNs in con

159 Activity is independent of NQO1/DT-diaphorase, maintained in drug-resistant cells and under

160 At the cellular level the NADPH-diaphorase marker for nNOS revealed a significant increa

161 y to heterodimeric [NiFe]-hydrogenases and a diaphorase moiety (HoxEFU) with homology to NuoEFG of re

162 ase as reflected in elevated steady state DT-diaphorase mRNA levels.

163 he existence of several distinct sizes of DT-diaphorase mRNA transcripts has been observed in human t

164 The crystal structure of human DT-diaphorase (NAD(P)H oxidoreductase (quinone); EC 1.6.99.

165 s that the two-electron quinone reductase DT-diaphorase [NAD(P)H:(quinone-acceptor) oxidoreductase, E

166 -nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH) histochemistry and SMI-32 immunocytoc

167 nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) activity and the distribution of bo

168 ession of specific, fixative-resistant NADPH-diaphorase (NADPH-d) activity, characteristic of NOS, wa

169 Recent evidence indicates that NADPH-diaphorase (NADPH-d) and nitric oxide synthase (NOS) can

170 nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemical techniques.

171 nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) histochemistry and conventional mic

172 -nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry and NOS immunocytoch

173 lysia californica was studied by using NADPH-diaphorase (NADPH-d) histochemistry in the CNS and perip

174 nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) histochemistry to identify the sour

175 nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) histochemistry were used to explore

176 of specific antibodies against NOS and NADPH-diaphorase (NADPH-d) histochemistry, which, with the exc

177 amide adenine dinucleotide phosphate reduced diaphorase (NADPH-d) histochemistry.

178 Hirudo medicinalis, were studied using NADPH-diaphorase (NADPH-d) histochemistry.

179 nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry.

180 Nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) is a key enzyme in the synthesis of

181 ornica was studied histochemically via NADPH-diaphorase (NADPH-d) reduction of Nitro Blue Tetrazolium

182 nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) to identify neurons of the laterodo

183 nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) was also used to characterize NOS-c

184 he normal distribution of constitutive NADPH-diaphorase (NADPH-d), a marker for nitric oxide synthase

185 nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d), glutamic acid decarboxylase (GAD),

186 esence and subcellular distribution of NADPH diaphorase (NADPH-d)/nitric oxide synthase (NOS) in the

187 nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d, an index of constitutive NOS) react

188 Formaldehyde-insensitive NADPH diaphorase (NADPHd) activity is used widely as a histoch

189 nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) activity was determined histochemica

190 amide adenine dinucleotide phosphate (NADPH)-diaphorase (NADPHd) and parvalbumin (PV)-positive cells

191 hase (nNOS) and enzymatic activity for NADPH diaphorase (NADPHd) are extensively colocalized in stria

192 NADPH-diaphorase (NADPHd) has been determined biochemically an

193 ng (IFL) methods, and each followed by NADPH diaphorase (NADPHd) histochemical staining in the same s

194 nicotinamide adenine dinucleotide phosphate-diaphorase (NADPHd) histochemistry and nitric oxide synt

195 nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) histochemistry or immunocytochemistr

196 NADPH-diaphorase (NADPHd) histochemistry or NOS-immunostaining

197 nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) histochemistry, a marker of nNOS act

198 albumin (PV) and nitric oxide synthase NADPH diaphorase (NADPHd) is well documented within neurons of

199 Nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) staining patterns in the nucleus tra

200 nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd)-reactivities in the sphenopalatine g

201 nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd, a marker for nitric oxide synthase)

202 nicotinamide adenine dinucleotide phosphate diaphorase (NDP) activity, a marker of nNOS, were concen

203 es were present in almost all cortical NADPH-diaphorase neurons and in approximately 50% of the spare

204 Nicotinamide adenine dinucleotide phosphate-diaphorase neurons were reduced in superficial WM and sh

205 ore prominent as nuclear inclusions in NADPH-diaphorase neurons, with less perikaryal and neuropil ag

206 ric and submucosal plexus stained with NADPH diaphorase (neurons and neurites), anti-TuJ1 (neurons an

207 A few VIP+ and NADPH- diaphorase+ neurons were also observed in the choroid.

208 activation of the chemotherapeutic drugs (DT-diaphorase, nicotinamide adenine dinucleotide phosphate:

209 NAD(P)H:quinone oxidoreductase 1 (EC; DT-Diaphorase, NQO1) is predominantly a cytosolic flavoenzy

210 ase in the number of cells labeled for NADPH diaphorase or neuronal NOS in the lumbosacral spinal cor

211 th little or no colocalization between NADPH-diaphorase or nitric oxide synthase neurons and huntingt

212 Axons labeled for VIP, nNOS, NADPH-diaphorase, or the 3A10 antigen could be traced from the

213 iatal neurones and the degeneration of NADPH-diaphorase positive interneurones within 24 h.

214 (nicotinamide adenine dinucleotide phosphate diaphorase) positive neurons and brain nitric oxide synt

215 ivity was in accordance with decreased NADPH-diaphorase-positive cells and decreased staining of NOS-

216 In contrast, a similar loss of NADPH-diaphorase-positive cells was observed in the striatum o

217 NADPH-diaphorase-positive cells were also increased in the ips

218 , the deep dorsal horn contained a number of diaphorase-positive cells, whereas the superficial dorsa

219 g and ventrally originating (U-shaped group) diaphorase-positive dorsal horn interneurons.

220 efferent fibers and to localize these NADPH-diaphorase-positive efferent cell bodies in the turtle b

221 he locus coeruleus corresponded to the NADPH-diaphorase-positive efferent cells in the avian isthmo-o

222 h P-CREB-lir was induced by light were NADPH-diaphorase-positive neurons of the SCN's retinorecipient

223 nNOS immunostaining and NADPH-diaphorase-positive neurons were significantly increased

224 cells, including GABAergic, cholinergic and diaphorase-positive neurons which were all destined to d

225 At both dorsal and ventral levels, NADPH-diaphorase-positive subicular pyramidal cells and CA1 no

226 nglia, total neurons per ganglion, and NADPH diaphorase presumptive inhibitory neurons per ganglion a

227 The presence of DT-diaphorase prevented the oxidation of reduced CoQ and in

228 nstruct, we found that two regions of the DT-diaphorase promoter region, positions -346 to -588 (cont

229 ltransferase construct containing 3 kb of DT-diaphorase promoter sequence.

230 The NADPH-diaphorase reaction was also used as a marker for NOS an

231 for NOS2, under assay conditions wherein the diaphorase reaction was strictly dependent on NOS2 expre

232 mide-adenine dinucleotide phosphate (NADPH)- diaphorase reaction was used as a marker for nitric oxid

233 amide adenine dinucleotide phosphate (NADPH)-diaphorase reaction, we determined that the organization

234 To determine the mechanism of these "diaphorase" reactions, we generated the EH(2) and EH(4)

235 Seven classes of diaphorase-reactive mPFC neurone are described; these ce

236 tudies have mapped the distribution of NADPH-diaphorase-reactive neurons in the hippocampal formation

237 f controversy concerns the presence of NADPH-diaphorase-reactive pyramidal cells in the CA1 subfield

238 ts show that nNOS immunoreactivity and NADPH-diaphorase reactivity are consistently increased in the

239 nicotinamide adenine dinucleotide phosphate diaphorase reactivity in microvessels, as well as the pr

240 nNOS immunostaining and NADPH-diaphorase reactivity was neither altered in the gracile

241 ibiting both nNOS immunoreactivity and NADPH-diaphorase reactivity was present in the central, medial

242 Diaphorase reactivity was very infrequently colocalised

243 nNOS expression and NADPH-diaphorase reactivity were quantified by using a microsc

244 ) significantly decreases k(cat)/K(m) for DT-diaphorase reductase activity for both PBIs and APBIs.

245 was to take advantage of stereoselective DT-diaphorase reductive activation as well as hydrogen bond

246 eaction of glucose-6-phosphate (G6P) and the diaphorase-resazurin amplifying system, we have develope

247 DNA-damaging species, and selectivity for DT-diaphorase-rich cells in vitro.

248 essential for potency and selectivity to DT-diaphorase-rich cells under aerobic conditions.

249 neurons, and whole-mount staining with NADPH-diaphorase showed that myenteric and submucosal ganglia

250 ide adenine dinucleotide in its reduced form-diaphorase stain, which is specifically used to confirm

251 Diabetic mice had loss of NADPH diaphorase-stained myenteric neurons, delayed gastric em

252 NADPH diaphorase staining (NOS index) intensity was higher in

253 NADPH-diaphorase staining also was detected in blood vessels o

254 ucing neurons using fixation-resistant NADPH-diaphorase staining and antisera that recognize a NOS-sp

255 wever, between nNOS immunostaining and NADPH-diaphorase staining in blood vessels in the brainstem.

256 onstrated by in situ hybridization and NADPH diaphorase staining in rats treated with TGF-beta1.

257 d arteries showed a 2-fold increase in NADPH-diaphorase staining intensity relative to sham-infected

258 O level in vitro but produces citrulline and diaphorase staining reflecting in vivo NOS activity in p

259 exhibiting NOS activity as assessed by NADPH-diaphorase staining was significantly greater in the PVN

260 nicotinamide adenine dinucleotide phosphate-diaphorase staining was unaltered, and no changes in NO

261 NADPH diaphorase staining was visible in both neuronal perikar

262 and 25, three defined bands of diffuse NADPH diaphorase staining were located in layer 2 and in upper

263 nitric oxide synthase (NOS) activity (NADPH-diaphorase staining), neuronal NOS (nNOS) protein, and n

264 endent of cell volume, correlates with NADPH-diaphorase staining, and appears to be a characteristic

265 itory neurotransmitter NO, as shown by NADPH-diaphorase staining, and the glial marker GFAP.

266 Diaphorase staining, anti-NO synthase (NOS) immunocytoch

267 dorsal tegmental nucleus identified by NADPH diaphorase staining, as well as the cuneiform nucleus an

268 s exhibiting nNOS immunoreactivity and NADPH-diaphorase staining.

269 and in approximately 50% of the spared NADPH-diaphorase striatal neurons from early grade HD cases.

270 -position of the PBIs and APBIs influence DT-diaphorase substrate activity to a lesser degree.

271 es 1-9 were studied with respect to their DT-diaphorase substrate activity, DNA reductive alkylation,

272 The influence of structure on DT-diaphorase substrate activity, topoisomerase II inhibiti

273 one ring, which was predicted to diminish DT-diaphorase substrate activity.

274 th respect with respect to the following: DT-diaphorase substrate design, DT-diaphorase-cytotoxicity

275 er rate-limiting for substrates with high DT-diaphorase substrate specificities.

276 High DT-diaphorase substrate specificity is not desirable in the

277 strates occurs with EH(2) while reduction of diaphorase substrates occurs with EH(4).

278 e involved in learning and memory, the NADPH-diaphorase technique was used in conjunction with immuno

279 uces toxicity by redox cycling with cellular diaphorases, thereby elevating intracellular levels of s

280 a bi-enzymatic system (a dehydrogenase and a diaphorase, this latter being useful to the safe regener

281 mitomycin C induces the overexpression of DT-diaphorase through a mechanism involving both the AP-1 a

282 Addition of NADH and DT-diaphorase to either large unilamellar or multilamellar

283 as determined on sections stained with NADPH diaphorase to identify the cholinergic boundaries of the

284 The ability of DT-diaphorase to maintain the reduced state of CoQ and prot

285 mg/m2 mitomycin C (MMC), the induction of DT-diaphorase transcripts was demonstrated.

286 ide adenosine dinucleotide phosphate (NADPH)-diaphorase, tyrosine hydroxylase (TH), and dopamine beta

287 r electrons were generated per glucose via a diaphorase-vitamin K(3) electron shuttle system at the a

288 st perfect co-localization of ChAT and NADPH-diaphorase was also observed.

289 ron acceptor, an artifactual activity for DT-diaphorase was detected in these cell lines.

290 DT-diaphorase was isolated and purified from rat liver cyto

291 fibers that stained for both nNOS and NADPH-diaphorase was noted in the interstitial and ventromedia

292 The suggestion is offered that DT-diaphorase was selected during evolution to perform this

293 nicotinamide adenine dinucleotide phosphate diaphorase was used to identify potential NO synthase ac

294 Nerve terminals positive for NADPH- diaphorase were colocalized with SM alpha-actin-positive

295 Thus excellent polycyclic substrates of DT-diaphorase were designed.

296 nes, and phenindone in the active site of DT-diaphorase were predicted by results from our inhibitor-

297 ining choline acetyltransferase and/or NADPH diaphorase were studied in E12.5-E17.5 reeler and wild-t

298 (P-Path), and the granule cell marker NADPH-diaphorase, were disrupted.

299 by HMP exceeding the one earlier shown with diaphorase, which makes HMP very attractive as a compone

300 The molecular basis of the interaction of DT-diaphorase with a cytotoxic nitrobenzamide CB1954 [5-(az