ライフサイエンスコーパス: propidium

1 tion, ethidium, but not its divalent analog, propidium.

2 We assayed propidium(2+) (Pro(2+)) influx kinetics during NLRP3 or

3 lux reaction, pointing to electrogenic 3H(+)/propidium(2+) antiport.

4 ptide aggregation and are equivalent only to propidium, a well-characterized AChE peripheral anionic

5 ructurally different planar drugs, ethidium, propidium and dequalinium.

6 as tetraphenylphosphonium (TPP+), ethidium, propidium and dequalinium.

7 n transport and binding of divalent cationic propidium and monovalent cationic ethidium.

8 These relative changes in propidium and tacrine affinities thus provided a sensiti

9 ing competitive inhibition constants KI2 for propidium and tacrine, inhibitors specific for the P- an

10 Whereas D235 and E327 were both involved in propidium binding, the loss of one of these carboxylates

11 es of DNA intercalators, including ethidium, propidium, daunorubicin, and adriamycin.

12 MTX treatment led to biphasic propidium dye uptake and dilated blebbing coincident wit

13 pulses (50 Hz, n = 3-100) and quantified by propidium dye uptake within 11 min after the nsPEF expos

14 P2X5 receptors also rapidly accumulated the propidium dye YO-PRO-1 in response to ATP.

15 h resulted in loss of electrogenicity in the propidium efflux reaction, pointing to electrogenic 3H(+

16 considerably more resistant to inhibition by propidium, ethopropazine, and eserine than is ChE2.

17 The exclusion of propidium, expression of EBV LTIII RNAs and proteins, an

18 A acetylation by a factor a(2) of 1.3, while propidium failed to accelerate.

19 Moreover, they displace propidium from the peripheral anionic site of AChE, prev

20 r percentages of late apoptotic Annexin V(+) propidium-idodide(+) liver-infiltrating MNCs and splenoc

21 Values of KI2 for propidium increased 30- to 100-fold when ligands had eit

22 served binding free energies of ethidium and propidium into five underlying contributions.

23 6-diamidino-2-phenylindole dihydrochloride), propidium iodide (3,8-diamino-5-[3-(diethylmethylammonio

24 Cardiomyocyte viability was quantified with propidium iodide (5 micromol/L), and production of free

25 ity was measured using fluorescein diacetate/propidium iodide (FDA/PI) cell viability assay.

26 he intracellular concentration of Ca(2+) and propidium iodide (PI) and the delivery of 3 kDa dextran

27 ther development, using anthers stained with propidium iodide (PI) and/or 5-ethynyl-2'-deoxyuridine (

28 ial transmembrane potential distribution and propidium iodide (PI) dye diffusion experiments demonstr

29 lic uptake of Hst 5 that invariably preceded propidium iodide (PI) entry, demonstrating that transloc

30 n uptake of the non-vital fluorescent marker propidium iodide (PI) of 150-500% above control levels,

31 eration was determined by direct counting of propidium iodide (PI) or 4',6'-diamino-2-phenylindole (D

32 In fixed lenses, DNA was stained with propidium iodide (PI) or 4',6-diamidino-2-phenylindole,

33 it is generally assumed that probes, such as propidium iodide (PI) or 7-amino-actinomycin D (7-AAD),

34 tic based on bromodeoxyuridine (BrdU) assay, propidium iodide (PI) staining and growth curves, and bl

35 WST-1 cytotoxicity assay and annexin V-FITC/propidium iodide (PI) staining as apoptosis-necrosis ass

36 Propidium iodide (PI) staining of the chamber neutrophil

37 Analysis by annexin V/propidium iodide (PI) staining revealed that the concent

38 antly necrotic as indicated by annexin V and propidium iodide (PI) staining, absence of caspase activ

39 ptosis was measured using annexin V-FITC and propidium iodide (PI) staining, and DNA fragmentation.

40 in 8 of 10 CLL samples measured by annexin V/propidium iodide (PI) staining.

41 We have used propidium iodide (PI) to investigate the dynamic propert

42 competence, and mounted in medium containing propidium iodide (PI) to visualize all nuclei.

43 e S-phase), and mounted in medium containing propidium iodide (PI) to visualize all nuclei.

44 showed conspicuous cell death as measured by propidium iodide (PI) uptake and chromatin condensation,

45 rogenase (LDH) release in culture medium and propidium iodide (PI) uptake in slices were used to eval

46 ols as assessed by Trypan Blue exclusion and propidium iodide (PI) uptake on a flow cytometer.

47 solated primary HSCs; data using fluorescent propidium iodide (PI) uptake revealed that leptin, like

48 ctate dehydrogenase (LDH) release in medium, propidium iodide (PI) uptake, and Nissl staining as mark

49 In addition, phosphatidylcholine (PC) and propidium iodide (PI) were used as the cell membrane and

50 h was associated with increased Annexin-V(+)/propidium iodide (PI)(-) cells, cleaved PARP, cleaved ca

51 cell wall fluorescence in cells stained with propidium iodide (PI), and (3) changes in apical wall fl

52 rescent plasma membrane integrity indicator, propidium iodide (PI), in HL60 human leukemia cells resu

53 culture with fluorescein diacetate (FDA) and propidium iodide (PI), respectively, showed a clear pred

54 LIVE/DEAD staining kit, based on Syto 9 and propidium iodide (PI), was also applied to assess cell e

55 n detection of active caspase 1 (Casp1)- and propidium iodide (PI)-positive cells.

56 eously with the fluorescent stains SYTO9 and propidium iodide (PI).

57 ) single-positive cells that bind AV but not propidium iodide (PI); and (b) double-positive cells tha

58 he authors used the positively charged dyes, propidium iodide (PrI) and 4'-6-diamidino-2-phenylindole

59 incubation to label nuclei (Hoechst 33342 & propidium iodide [PI]); cytosol (CellTracker Red CMTPX,

60 showing positive staining for annexin V and propidium iodide after antisense treatment was 40% at 28

61 icroscopy for viability, after staining with propidium iodide and acridine orange.

62 ssed either as whole mounts and stained with propidium iodide and an antibody against alpha9 integrin

63 osis in tumor-bearing mice was detected with propidium iodide and annexin V staining.

64 evels of thymic apoptosis were determined by propidium iodide and annexin V staining.

65 flow cytometry analysis after staining with propidium iodide and annexin V, we also evaluated the cy

66 Staining of MCF13 MLV-infected cells with propidium iodide and annexin V-fluorescein isothiocyanat

67 -2 H-tetrazolium assay, cell cycle analysis, propidium iodide and annexin-V staining, and caspase-3-m

68 observed rapid membrane permeabilization to propidium iodide and ATP efflux in response to C4.

69 nd polarization were measured using the dyes propidium iodide and bis-(1,3-dibutylbarbituric acid) tr

70 dation) were measured fluorometrically using propidium iodide and chloromethyl dihydrodichlorofluores

71 Further, acridine orange, ethidium bromide, propidium iodide and DAPI staining demonstrated that cel

72 embrane tracers with graded molecular sizes (propidium iodide and FITC-dextrans with molecular sizes

73 for 24 hr before flow cytometric analysis of propidium iodide and fluorescein isothiocyanate-conjugat

74 The cells were labeled with Syto 9 and propidium iodide and imaged through a fluorescent micros

75 d results in increased apoptosis as shown by propidium iodide and JC-1 staining.

76 the membrane impermeable fluorescent marker propidium iodide and randomized to one of four ventilati

77 ed number of cells that stained positive for propidium iodide and reduced apoptotic markers.

78 Staining with propidium iodide and Syto 16 revealed a decrease in viab

79 ced apoptosis in DAOY cells as determined by propidium iodide and terminal deoxynucleotidyltransferas

80 s confirmed by viable cell counts, annexin V/propidium iodide and tetramethyl-rhodamine ethylester st

81 In addition, a reduction in the uptake of propidium iodide and the number of apoptotic nuclei and

82 jejunum were stained with Hoechst 33342 and propidium iodide and then sorted using fluorescence-acti

83 ain cytoplasmic membrane integrity, blocking propidium iodide and Trypan blue.

84 anginex caused endothelial cells to take up propidium iodide and undergo depolarization, both parame

85 -mediated dUTP nick-end labeling (TUNEL) and propidium iodide and with anti-von Willebrand factor, an

86 assessed by the permeability of dextran and propidium iodide as well as by measuring the transendoth

87 cross-linking, gp350-positive cells excluded propidium iodide as well as gp350-negative cells.

88 esult of a fluorescent microscopic annexin V/propidium iodide assay, performed in microfluidics, conf

89 induces apoptosis, assayed by the supravital propidium iodide assay, through modulation of the apopto

90 Annexin V and propidium iodide assays demonstrated that SingleBond ind

91 in cell death, as measured by alamarBlue and propidium iodide assays, respectively.

92 cated by PARP-1, caspases 3/7, and annexin V/propidium iodide assays.

93 ssays, including Western blotting, annexin-V/propidium iodide binding, comet, and micronuclei assays,

94 ere analyzed for expression of annexin-V and propidium iodide by flow cytometry.

95 ell death was measured by using a calcein-AM/propidium iodide cell-survival assay.

96 Staining of infected cells with propidium iodide demonstrated that M. tuberculosis induc

97 ung epithelial cells, as measured by annexin/propidium iodide detection by flow cytometry.

98 cell death (determined by failure to exclude propidium iodide dye).

99 ular integrity as measured by trypan blue or propidium iodide exclusion and [ATP].

100 ))-dependent cytotoxicity was observed using propidium iodide exclusion and annexin V staining.

101 d cell death to 25.4% compared with control (propidium iodide exclusion assay, P<0.001).

102 optosis, as confirmed by annexin V staining, propidium iodide exclusion, and identification of cells

103 iazolyl blue tetrazolium bromide methods and propidium iodide exclusion, gene expression by real-time

104 nce assay (Promega, Madison, WI, USA) and by propidium iodide exclusion.

105 Annexin-propidium iodide flow cytometry assays, cell morphology

106 eoxyuridine, a thymidine analog) and annexin-propidium iodide flow cytometry was performed to determi

107 lungs labeled during injurious ventilation, propidium iodide fluorescence identifies all cells with

108 in lungs labeled after injurious ventilation propidium iodide fluorescence identifies only cells with

109 luorescence plate scanner equipped to detect propidium iodide fluorescence.

110 14 days, and neuronal damage assessed using propidium iodide fluorescence.

111 Cell viability was determined by way of propidium iodide fluorometry.

112 ccompanied by an enhanced cellular uptake of propidium iodide in a Ca(2+)- and ROCK-dependent manner

113 size of conjunctival follicles stained with propidium iodide in rabbits ranging in age from 2 days t

114 e identified as those that were stained with propidium iodide in such populations.

115 ase activation, and membrane permeability to propidium iodide in the absence and presence of sPLA(2).

116 Propidium iodide influx assay demonstrated the lysis of

117 tocellular injury was assessed by histology, propidium iodide injection, and alanine aminotransferase

118 The injection of propidium iodide into either endothelial or smooth muscl

119 d from the spleen and liver at necropsy, and propidium iodide labeled target-specific cytolysis was d

120 otic eosinophils was determined by annexin V-propidium iodide labeling, and CD30 expression was exami

121 the gain of pyknotic nuclear morphology and propidium iodide labeling.

122 Apoptosis was measured by annexin V/propidium iodide labeling.

123 longest applied pulses, immediate uptake of propidium iodide occurred consistent with electroporatio

124 occurred with significantly later uptake of propidium iodide occurring after 60 ns pulses compared t

125 Samples were mounted with propidium iodide or DAPI.

126 or BrdU and/or Ki-67 and counterstained with propidium iodide or Syto 59.

127 een fluorescent protein, and costaining with propidium iodide revealed a predominantly nucleolar loca

128 Cell cycle analysis with propidium iodide revealed that CD11b expression at 24 h

129 , staining with the cell viability indicator propidium iodide revealed that Zn2+ is responsible for t

130 ce resulting from exposing sampled tissue to propidium iodide solution 16-24 h after sampling.

131 ncer cells has been determined via Annexin V/Propidium iodide stain and flow cytometry.

132 ty (relative fluorescence), and cellularity (propidium iodide stain).

133 ble as determined by differential Syto 9 and propidium iodide staining after MazF(Sa) induction.

134 Cell death was measured by Hoechst/propidium iodide staining and activation of caspase-3.

135 related with rRNA transcription, as shown by propidium iodide staining and BrUTP incorporation.

136 sorafenib-induced apoptosis as determined by propidium iodide staining and by assessing the mitochond

137 r a 18-h period as assessed by Hoechst 33342/propidium iodide staining and caspase-3 and -9 activatio

138 tosis of freshly isolated IEC as assessed by propidium iodide staining and DNA laddering.

139 cycle by bromodeoxyuridine incorporation or propidium iodide staining and flow cytometry and measure

140 Anoikis was quantified by YO-PRO-1/propidium iodide staining and flow cytometry.

141 Cell viability was monitored with propidium iodide staining and lactate dehydrogenase rele

142 -mediated dUTP-biotin nick end labeling, and propidium iodide staining assays, it was shown that rSV5

143 bodies and quantified by a cell death assay (propidium iodide staining in the subdiploid peak) or cel

144 treated neutrophils was determined using the propidium iodide staining method.

145 s, and monitored cell death by annexin V and propidium iodide staining of lymphocytes, using flow cyt

146 BrdUrd incorporation and propidium iodide staining of prostate LNCaP cells arrest

147 Propidium iodide staining revealed that KB1050 accumulat

148 G(2) cell cycle arrest as determined by propidium iodide staining was not a result of mitotic ar

149 n assay, and annexin V binding combined with propidium iodide staining was used for the distinction o

150 assayed for annexin V binding, DNA content (propidium iodide staining), and DNA fragmentation (termi

151 , and increases cell death (as determined by propidium iodide staining).

152 is of a lactate dehydrogenase release assay, propidium iodide staining, and measurement of the total

153 , G(2)/M accumulation, typically assessed by propidium iodide staining, begins to be measurable only

154 early cell cycle entry; this was assessed by propidium iodide staining, CFSE labeling profiles, [(3)H

155 aining of select yeast cells which also show propidium iodide staining, indicating ZCOE is a "dead" s

156 th based on early LDH release, annexin V and propidium iodide staining, morphological changes of infe

157 Conversely, propidium iodide staining, PARP cleavage patterns, and r

158 death in the CA1 region was quantified using propidium iodide staining.

159 bicin, or H2O2 and was measured by annexin V/propidium iodide staining.

160 le with TUNEL (Roche) and dual annexin V and propidium iodide staining.

161 T cells, as judged by reduction in annexin V/propidium iodide staining.

162 nfirmed with cell cycle analysis and annexin-propidium iodide staining.

163 tic cell death was measured by annexin V and propidium iodide staining.

164 ound cells were identified by differences in propidium iodide staining.

165 cted by [(3)H]thymidine incorporation and by propidium iodide staining.

166 ndritic cells was evaluated by annexin-V and propidium iodide staining.

167 using a green fluorescent nucleic acid stain/propidium iodide staining.

168 ad decreased membrane integrity, as shown by propidium iodide staining.

169 primarily necrotic as judged using Annexin V/propidium iodide staining.

170 pe (TEM), as well as the nuclear labeling by propidium iodide staining; terminal deoxynucleotidyl tra

171 Using propidium iodide to label nuclei and 5-bromo-2'-deoxyuri

172 hesis by immunofluorescence and stained with propidium iodide to measure DNA content by fluorescence-

173 e M-phase), and mounted in medium containing propidium iodide to visualize all nuclei.

174 tericidal effect on H. pylori as revealed by propidium iodide uptake and a morphological shift from s

175 Cell death and apoptosis were quantified by propidium iodide uptake and annexin-V staining, respecti

176 Based on propidium iodide uptake and cell morphology, the majorit

177 Propidium iodide uptake assays were used to examine acut

178 Propidium iodide uptake highly correlated with cell viab

179 ase in neuronal death assessed 24 h later by propidium iodide uptake in dead cell nuclei.

180 s to CORT and NMDA synergistically increased propidium iodide uptake in each hippocampal region, effe

181 Exposure to NMDA caused significant propidium iodide uptake in each hippocampal region, whil

182 te on neuronal cell death using fluorescence propidium iodide uptake in rat organotypic hippocampal-e

183 For nanosecond pulses, more delayed propidium iodide uptake occurred with significantly late

184 Experimental measurements of propidium iodide uptake provided evidence of a real memb

185 luciferase reporter), and cell necrosis (via propidium iodide uptake).

186 NEL positivity, phosphatidylserine exposure, propidium iodide uptake, and caspase-3 cleavage.

187 increases in phosphatidylserine exposure and propidium iodide uptake, was also inhibited by cariporid

188 privation was neuroprotective as measured by propidium iodide uptake, with an EC(50) between 1 and 10

189 xposure alone did not significantly increase propidium iodide uptake.

190 oxicity assessed by fluorescent detection of propidium iodide uptake.

191 failed to reduce the significant increase in propidium iodide uptake.

192 s rapid adenosine triphosphate depletion and propidium iodide uptake.

193 ly 30% of cultured EC to die, as assessed by propidium iodide uptake.

194 later, neuronal death was again assessed by propidium iodide uptake.

195 membrane asymmetry (annexin V staining), and propidium iodide uptake.

196 reactive oxygen species (ROS) production and propidium iodide uptake.

197 ra-AM] abolished cytotoxicity as measured by propidium iodide uptake.

198 ssessed by lactate dehydrogenase leakage and propidium iodide uptake.

199 easured by lactate dehydrogenase leakage and propidium iodide uptake.

200 Syncytia were detected by DNA staining with propidium iodide using flow cytometry to determine cell

201 (approximately 100 nM), while the uptake of propidium iodide was absent.

202 The increase in membrane permeability to propidium iodide was accompanied by a two- to threefold

203 lls, membrane permeability as measured using propidium iodide was greater in the presence of AbiZ.

204 r staining with the membrane impermeable dye propidium iodide was observed immediately following kain

205 nutes at high tidal volume settings, whereas propidium iodide was perfused either during or after inj

206 MDAR-dependent neuronal death as assessed by propidium iodide was similar with both co-agonists.

207 s an indicator of microvascular leakage, and propidium iodide was used to stain for irreversibly inju

208 No necrotic cells labeled with propidium iodide were detected in moribund animals on da

209 Fluo-3 and propidium iodide were employed to evaluate calcium fluxe

210 orimetric assay, based on the interaction of propidium iodide with DNA, that allows either real-time

211 asured outcomes included cell viability (via propidium iodide) and oxidant generation (reactive oxyge

212 cl-xL, lactate dehydrogenase, annexin V, and propidium iodide) nor VEGF or TGF-beta levels, but siIL-

213 islet viability (>90% fluorescein diacetate/propidium iodide) or the insulin secretion profile in dy

214 permeant (calcein) and membrane impermeant (propidium iodide) stains.

215 Live/dead (calcein AM and propidium iodide) testing revealed that a certain fracti

216 mic group had significantly more cell death (propidium iodide) than non-ischemic controls at 24 hr an

217 m (P<0.05) while intercellular dye transfer (propidium iodide) was maintained.

218 to ACh and labeling of disrupted cells with propidium iodide), an air bubble was perfused through a

219 striction to phenylephrine and labeling with propidium iodide), FCD was perifused around the vessel a

220 , a membrane-impermeable nucleic acid stain (propidium iodide), or a fluorescein-labeled antibody and

221 cellular viability (calcein AM and annexin-V/propidium iodide), reactive oxygen species (ROS; mitosox

222 and duplex-binding fluorophores (Hoechst or propidium iodide).

223 es of nonphagocytosed Annexin V+, TUNEL+, or propidium iodide+ apoptotic thymocytes suggests there is

224 When labelled with the fluorescent dye propidium iodide, 68 and 36 cells were identified as smo

225 the protein competes the interaction between propidium iodide, a DNA-binding dye, and apoptotic cells

226 s study we used real-time uptake patterns of propidium iodide, a fluorescent cell impermeable model d

227 Annexin V, propidium iodide, and acridine orange staining were meas

228 cal/multiphoton microscopy of rhodamine 123, propidium iodide, and calcein.

229 at 5, 10, 15, 28, and 56 days, stained with propidium iodide, and observed (layer by layer) by confo

230 ARPE19 was determined using monotetrazolium, propidium iodide, and TUNEL assays, and Zn(2+) uptake wa

231 nd cellular immunofluorescence staining with propidium iodide, anti-Annexin V and DAPI.

232 ransient permeabilization of 83% of cells to propidium iodide, cells placed at 37 degrees C resealed

233 Chondrocyte nuclei were stained with propidium iodide, examined by fluorescence microscopy, a

234 ium bromide (MTT) assay, flow cytometry with propidium iodide, gene expression profiling, RT-PCR, and

235 Cells were fixed and stained with propidium iodide, imaged using a confocal microscope, an

236 with use of the non-vital fluorescent marker propidium iodide, in organotypic slice cultures of male

237 by PMNs, and internalized bacteria excluded propidium iodide, indicating intact bacterial membranes.

238 Neuronal injury was quantified using propidium iodide, which becomes fluorescent only when it

239 orescence-activated cell sorting analysis of propidium iodide- and annexin V-stained transfected cell

240 confocal microscopy in cells recorded with a propidium iodide-containing electrode for longer than 30

241 Flow cytometric analysis of annexin V- and propidium iodide-labeled cells showed a marked induction

242 nd flow cytometry showed increased annexin V/propidium iodide-labeled cells when grown on AGE-Matrige

243 -treated cells undergo an annexin V-positive/propidium iodide-negative phase of death consistent with

244 cell injury was quantified as the number of propidium iodide-positive cells per alveolus.

245 sporin A significantly reduced the number of propidium iodide-positive ePTFE and Dacron adherent neut

246 the CNS showed significantly fewer annexin V/propidium iodide-positive lymphocytes in the CNS of P2X7

247 enase release from cells, and an increase in propidium iodide-positive nuclei in response to thapsiga

248 Flow cytometry analysis of annexin-V/propidium iodide-stained cells revealed that PlGF and Pl

249 IH, Bethesda, MD) to count Ki67-positive and propidium iodide-stained cells.

250 s matrix that was positive when stained with propidium iodide.

251 oton microscopy of rhodamine 123 (Rh123) and propidium iodide.

252 ion containing the membrane-impermeant label propidium iodide.

253 ells as measured by their ability to exclude propidium iodide.

254 ional binding of annexin V and the uptake of propidium iodide.

255 s measured using annexin V-phycoerythrin and propidium iodide.

256 l injury was measured fluorometrically using propidium iodide.

257 and </=4% of the monocytes were stained with propidium iodide.

258 ed using the fluorescent stains SYBER-14 and propidium iodide.

259 s suspended in physiologic buffer containing propidium iodide.

260 es by demonstrating their ability to exclude propidium iodide.

261 sulted in uptake of membrane-impermeable dye propidium iodide.

262 toskeletal proteins, and counterstained with propidium iodide.

263 later by staining with the cell-death marker propidium iodide.

264 insensitive to the peripheral site inhibitor propidium iodide.

265 ession were analyzed by flow cytometry using propidium iodide.

266 response to acetylcholine and labelling with propidium iodide.

267 ge/ethidium bromide or annexin-V-fluorescein/propidium iodide.

268 sured by tumor cell binding to Annexin V and propidium iodide.

269 cycle phase were tested by staining DNA with propidium iodide.

270 % (n = 7) of the neutrophils were stained by propidium iodide.

271 yrene surfaces for 6 hours were positive for propidium iodide.

272 nsitivity to the 'peripheral site' inhibitor propidium iodide.

273 l cycle, as indicated by flow cytometry with propidium iodide.

274 rmeability to the vital dyes trypan blue and propidium iodide.

275 dye YO-PRO-1 while remaining impermeable to propidium iodide.

276 ralleled by the uptake of the pannexin probe propidium iodide.

277 sts on new and treated disks were assayed by propidium iodide/DNA stain assay and confocal microscopi

278 aliva) were examined with Hoechst dye 33342, propidium iodide/eithidium bromide, and FITC-annexin V t

279 However, the propidium iodide/Hoechst assay gives morphological infor

280 A combination of the sulforhodamine B and propidium iodide/Hoechst assays would provide the most a

281 The trypan blue assay and a microscope-based propidium iodide/Hoechst staining assay assess only late

282 Propidium iodide/RNAase staining and flow cytometry was

283 Counts of propidium-iodide-stained nuclei for 2.2 MPa open-chest M

284 part, enhanced PMN apoptosis, as assessed by propidium iodine staining and caspase-3 activation.

285 lar macrophages, as defined by annexin V and propidium iodine staining, respectively.

286 ed how small peripheral site ligands such as propidium may inhibit substrate hydrolysis.

287 fy green produce, we developed and applied a propidium monoazide (PMA) real-time PCR assay to quantif

288 real-time PCR (qPCR) technique combined with propidium monoazide (PMA) to simultaneously detect viabl

289 pendent detection of live cells was based on propidium monoazide (PMA) treatment to selectively remov

290 for the first time that the combination of a propidium monoazide (PMA) treatment with haRPA, the so-c

291 se background from killed organisms, we used propidium monoazide (PMA), a DNA-binding dye that penetr

292 Samples were treated with propidium monoazide to distinguish live from dead cells

293 tal 16S rRNA gene signatures as revealed via propidium monoazide treatment of the samples.

294 d on the photoreactive DNA-intercalating dye propidium monoazide(4).

295 classical inhibitors such as edrophonium and propidium or inhibitors that are current or potential dr

296 whereas 60% of cells placed on ice remained propidium-permeable even in 30 min.

297 Moreover, the binding of propidium resulted in a clear increase in kOP for EMPC,

298 electronic strain caused by the proximity of propidium to EMPC in the ternary complex may promote pho

299 Binding of the small ligand propidium to the AChE peripheral site decreased kOP/KOP

300 ocholine hydrolysis rates in the presence of propidium under nonequilibrium conditions were simulated