ライフサイエンスコーパス: calcein

1 es in the amplitudes and rates of release of calcein.

2 , and these cells exported the MRP substrate calcein.

3 ex and extracellular, but not intracellular, calcein.

4 tion in fibroblasts stained with Hoechst and calcein.

5 ence from mitochondrially targeted DsRed1 or calcein.

6 tion by quantifying the release of preloaded calcein.

7 lease and dequenching of the fluorescent dye calcein.

8 , than the small soluble fluorescent marker, calcein.

9 tion of hydrophobic Nile red and hydrophilic calcein.

10 scein, Oregon green 488 carboxylic acid, and calcein.

11 copy of rhodamine 123, propidium iodide, and calcein.

12 ptanol significantly reduced the movement of calcein (12+/-3%, n=6 co-cultures).

13 an for permanent mPTP, as neither Rhod-2 nor calcein (600 Da) were lost.

14 netics of metabolite exchange, we introduced calcein, a 623-Da fluorophore, into the Anabaena cytopla

15 ptides inhibited the BK-triggered release of calcein, a hemichannel-permeable dye.

16 Finally, we utilized sonoporation to deliver calcein, a membrane-impermeant substrate of multidrug re

17 harmacophore was generated for inhibition of calcein accumulation in P-gp expressing LLC-PK1 cells an

18 th data for inhibition of digoxin transport, calcein accumulation, vinblastine accumulation, and vinb

19 endothelial cells, as determined by cellular calcein accumulation.

20 The study demonstrated that Calcein acetoxymethyl (AM) proved to be a suitable dye f

21 euroblastoma cells was evaluated with 4-hour calcein acetoxymethyl ester (calcein-AM) microcytotoxici

22 Viable cells were labeled with calcein acetoxymethyl, visualized using fluorescent micr

23 demonstrated that, like MDR1, SPGP effluxed calcein-acetoxymethyl ester (AM).

24 acellular esterase activity were analyzed by calcein-acetoxymethyl ester (AM)/ethidium homodimer assa

25 placed in culture media containing 2 microM calcein-acetoxymethyl ester (calcein-AM) and 4 microM et

26 equently, cell survival was quantified using calcein-acetoxymethyl ester compound and a fluorescent p

27 tamate receptor antagonists, was measured by calcein-acetoxymethyl ester staining after 3 days in cul

28 ine, survival rates of RGCs were measured by calcein-acetoxymethyl ester staining.

29 osporine, plasma membrane integrity based on calcein-acetoxymethyl fluorescence was significantly gre

30 Calcein acetoxymethylester and ATP assays confirmed that

31 studies on uptake and efflux, inhibition of calcein acetoxymethylester efflux, alteration of ATP lev

32 s was determined by live cell staining using calcein AM (5 microM).

33 ompetitive inhibitor of daunorubicin (MRP1), calcein AM (P-gp), and pheophorbide A (BCRP) transport.

34 sured variables included cellular viability (calcein AM and annexin-V/propidium iodide), reactive oxy

35 small cell lung cancer cell line H69 AR in a calcein AM and daunorubicin cell accumulation assay.

36 lucose-6-phosphate dehydrogenase (G6DP), and calcein AM and ethidium homodimer (calcein AM/EthD-1)] h

37 Cell viability was measured using calcein Am and ethidium homodimer-1.

38 ide-containing derivatives promote uptake of calcein AM and have very slow passive, absorptive, and s

39 Thioamide 31-S promoted uptake of calcein AM and inhibited efflux of vinblastine with IC(5

40 Live/dead (calcein AM and propidium iodide) testing revealed that a

41 (10), and their ability to promote uptake of calcein AM and vinblastine in multidrug-resistant cells.

42 (10), for their ability to promote uptake of calcein AM and vinblastine in multidrug-resistant MDCKII

43 Cell viability was measured by calcein AM assay, and 2',7'-dichlorofluorescein diacetat

44 olayers, more than 30% of clone A cells lost calcein AM fluorescence compared to fewer than 5% of CX-

45 Cell volume was measured with the use of calcein AM fluorescent dye, detected by confocal microsc

46 measured in low-passage human SC cells using calcein AM fluorescent dye; images were captured with a

47 l cells from RCs was possible after 5 min of Calcein AM incubation.

48 Using the calcein AM method, at day 2, 10 nmol/l rapamycin caused

49 osome pool, of LeMDR1 were active in pumping calcein AM out of the cell.

50 as assessed by phase-contrast microscopy and calcein AM staining and quantified with imaging software

51 Pulse-chase labelling experiments with calcein AM suggested that the Golgi and ER pools, but no

52 Cells labelled with calcein AM under conditions that slow vesicular transpor

53 The viability dye calcein AM was unchanged in AD terminals compared to con

54 f the traceable-fluorescent LeMDR1 substrate calcein AM were examined in both Leishmania mexicana and

55 odide [PI]); cytosol (CellTracker Red CMTPX, calcein AM); and membranes (octadecyl rhodamine B chlori

56 (7)) were labeled with rhodamine-dextran and calcein AM, cultured with cells from one mouse liver in

57 er selective loading of the endothelium with calcein AM, direct transfer of dye from the endothelium

58 Calcein AM, the cell-permeable derivative of calcein, sh

59 The cell volume of calcein AM-loaded keratocytes and myofibroblasts was det

60 , Oregon green carboxylic acid diacetate, or Calcein AM.

61 unting cells in tissue colabeled with PI and Calcein AM.

62 6DP), and calcein AM and ethidium homodimer (calcein AM/EthD-1)] have been adopted to verify the feas

63 as assayed by BrdU uptake and cell counts of calcein AM/ethidium bromide-stained cells.

64 nduced apoptosis was further confirmed using calcein AM/ethidium homodimer-1 dye and cleavage of poly

65 , 7, 8, and 15 pi were labeled in vitro with calcein-AM (C-AM) and infused intravenously into syngene

66 etrogradely labeled RGCs was determined with calcein-AM 24 hours after plating.

67 ing P-gp overexpressing PLHC-1/dox cells and calcein-AM as model substrate.

68 With the calcein-AM assay, LA-N-1 cell survival was 10%, 55%, and

69 luated for P-glycoprotein inhibition using a calcein-AM assay.

70 Cell-to-cell transfer of the fluorescent dye calcein-AM confirmed cytoplasmic communication via nanot

71 Using calcein-AM efflux assay, we identified compound 28 (IC50

72 tility, and ABC-transporter inhibition via a calcein-AM efflux assay.

73 lly, the TMR analogues facilitated uptake of calcein-AM into CR1R12 and MDCK-MDR1 cells and are activ

74 luorescent calcein for over 60 minutes after calcein-AM is removed from the extracellular space.

75 roblasts, and B lymphoblastoid cell lines in calcein-AM retention NK assays with allogeneic NK effect

76 lthough cyclosporine A and reserpine blocked calcein-AM transport by MDR1, these drugs had either min

77 pite dramatic reduction in rhodamine 123 and calcein-AM transport, the linker-shortened mutant P-gp p

78 IgG was toxic to keratinocytes, as judged by calcein-AM uptake.

79 Living cells, determined by metabolism of calcein-AM viewed with fluorescein filters, were counted

80 aining 2 microM calcein-acetoxymethyl ester (calcein-AM) and 4 microM ethidium homodimer.

81 ted with 4-hour calcein acetoxymethyl ester (calcein-AM) microcytotoxicity assay, electron microscopy

82 led that one analog inhibited SPGP efflux of calcein-AM, although not as potently as ditekiren.

83 Proliferation was determined using calcein-AM, and cytotoxicity was evaluated by MTT assay.

84 transfected into Jurkat cells, labeled with Calcein-AM, and migration to SCF assessed in the presenc

85 bodipy-FL)-verapamil, bodipy-FL-vinblastine, calcein-AM, bodipy-FL-prazosin, bisantrene, and bodipy-F

86 ters export canonical MDR susbtrates such as calcein-AM, bodipy-verapamil, bodipy-vinblastine, and mi

87 times more of the ABC transporter substrates calcein-AM, CellTrace RedOrange, BoDipy-verapamil and Bo

88 rect observation and by adoptive transfer of calcein-AM-labeled bone marrow-derived leukocytes from s

89 odamine-stained glucose-signal amplifier and calcein-AM-stained pancreatic beta-cell capsules, is dev

90 ct, respectively, on blocking SPGP efflux of calcein-AM.

91 and preferentially inhibited SPGP efflux of calcein-AM.

92 Redox-active iron was monitored using calcein-AM.

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

94 nal but a decrease in background signal from calcein and 3'-(p-aminophenyl) fluorescein (APF) and no

95 Calcein and a tetracycline derivative (BoneTag agent [BT

96 sed the membrane-impermeable fluorescent dye calcein and alexa-dextran, with or without a calcium cha

97 Calcein and alizarin were injected 6 and 3 days, respect

98 hen ventricular myocytes were preloaded with calcein and co-cultured with myofibroblasts for 24 h, ca

99 rmine cell viability, cells were loaded with calcein and counted.

100 The results of the uptake of calcein and cytotoxicity of doxorubicin in human cervica

101 ectively), were loaded with the fluorochrome calcein and exposed to a range of concentrations of each

102 As estimated by calcein and Fe2+ chelator, the mean +/- SD labile Fe2+ c

103 In contrast, as estimated by calcein and Fe3+ chelator, total erythrocyte labile iron

104 ocal imaging, hepatocytes were coloaded with calcein and tetramethylrhodamine methyl ester to visuali

105 To address this need, uptake of calcein and viability of DU 145 prostate cancer cells we

106 The delivery of a membrane-impermeable dye (calcein) and a chemotherapeutic drug (doxorubicin) are d

107 somes encapsulating fluorescent calcein (f-L-calcein) and doxorubicin (f-L-DOX), respectively, which

108 fluorescence signals from membrane permeant (calcein) and membrane impermeant (propidium iodide) stai

109 We used the fluorescent metallosensor, calcein, and a permeant Fe2+ chelator to estimate labile

110 ence detection of a self-quenched green dye, calcein, and a reference red dye, sulforhodamine 101, af

111 mulation of MRP1 substrates, vincristine and calcein, and decreases in calcein efflux from intact MRP

112 d for evaluating cytotoxicity (MTS, CyQUANT, Calcein, and EthD-1) and oxidative stress (DCFH-DA and A

113 it and (b) mitochondria became permeable for calcein ( approximately 620 daltons) concurrently with d

114 r mitochondrial membrane to matrix-entrapped calcein (approximately 620 Da), indicating the opening o

115 luorescence of a mitochondria-entrapped dye, calcein, are observed coincidentally.

116 luation of the intracellular level of LIP by calcein assay revealed that both "basal" and "UVA-induce

117 Cell viability was assessed using calcein assay, and annexin V binding combined with propi

118 assessed with the use of dihydroethidium and calcein assays, respectively.

119 A calcein-based fluorescence quenching method was utilized

120 In this way Calcein Blue, newly free to fluoresce, contributes to gl

121 e in which a second fluorophore, in our case Calcein Blue, quenched by a cobalt ion is add to the fir

122 forms pores that allow the efflux of the dye calcein but not Dextran 3000.

123 king screening and identify a lead compound, calcein, capable of blocking TopBP1 oligomerization and

124 e, as the permeability of the small molecule calcein co-incubated with the protein-polymer conjugate

125 MPTP was determined using the calcein-cobalt technique.

126 of the LAMP reaction were detected using the calcein colorimetric method and further analysed via the

127 SIH) in rapidly releasing iron from the iron-calcein complex.

128 ength (0.05-20 ms), number of pulses (1-10), calcein concentration (10-100 microM), and cell concentr

129 ake was shown to vary linearly with external calcein concentration.

130 this happened in a non-lytic fashion, using calcein-containing vesicles as controls.

131 orescence studies with vesicles with trapped calcein demonstrate betaLG binding induces leakage in DM

132 All regions in CTL hearts exhibited faster calcein diffusion than in HF, with HF-AS myocyte being s

133 The release of calcein dye from liposomes induced by interactions with

134 en studied using a vesicle-disruption assay (calcein dye release) and electron microscopy.

135 , TBX18-NRCMs exhibited slowed intercellular calcein dye transfer kinetics (421 +/- 54 versus control

136 d the release from the matrix of sequestered calcein, effects prevented by the inhibitor of the PTP c

137 s, which overexpress MRP1, and monitored the calcein efflux by MRP1.

138 s, vincristine and calcein, and decreases in calcein efflux from intact MRP1-expressing human tumour

139 cient for insertion into lipid membranes and calcein efflux.

140 ith lipid model membranes were studied using calcein-encapsulated vesicle leakage, attenuated total r

141 MGDG could not be achieved as determined by calcein entrapment.

142 pithelial surface cells was examined using a calcein-ethidium assay.

143 The calcein-ethidium viability assay revealed that the norma

144 e-coated liposomes encapsulating fluorescent calcein (f-L-calcein) and doxorubicin (f-L-DOX), respect

145 The idea is that the maximum increase in calcein fluorescence after iontophoresis is proportional

146 By use of rabbit duodenal tissue, a calcein fluorescence assay has previously been developed

147 Iron regulatory protein bandshift and calcein fluorescence assays reveal decreased intracellul

148 -pumping adenosine triphosphatase, cytosolic calcein fluorescence became quenched.

149 nted by a 28+/-3% reduction in mitochondrial calcein fluorescence compared with control; P<0.01).

150 diation-induced ROS/RNS, depolarization, and calcein fluorescence decrease are inhibited by the mitoc

151 A narrow (<5 ms duration), intense spike of calcein fluorescence due to content release and dequench

152 ne potential and decreased the mitochondrial calcein fluorescence in a concentration- and time-depend

153 Bafilomycin also quenched calcein fluorescence in mitochondria, which was blocked

154 Cell-cell coupling was assessed by calcein fluorescence recovery after photobleach during i

155 nd co-cultured with myofibroblasts for 24 h, calcein fluorescence was detected in 52+/-4% (n=8 co-cul

156 resulted in an 50% loss of the mitochondrial calcein fluorescence, suggesting substantial activation

157 in living wild-type and AQP3-null mice using calcein fluorescence-quenching and 14C-glycerol-uptake a

158 rial membrane potential and in mitochondrial calcein fluorescence.

159 of control values after 12 hr as measured by calcein fluorescence.

160 on of host esterase activity, as measured by calcein fluorescence.

161 mical assay, ferritin induction, and loss of calcein fluorescence.

162 NPE cell volume can be measured with calcein-fluorescence quenching.

163 Cell volume changes were measured by calcein-fluorescence quenching.

164 n, a separate group of animals were fed with calcein fluorescent stain and processed for non-decalcif

165 The observed partial release of trapped calcein following activation of MscL was attributed to t

166 omethacin continue to accumulate fluorescent calcein for over 60 minutes after calcein-AM is removed

167 e N-terminal helix insertion, the release of calcein from erythrocyte ghosts, and hemolysis of erythr

168 e activity as measured by induced leakage of calcein from large unilamellar vesicles.

169 n and variants elicit an enhanced release of calcein from liposomes composed of the negatively-charge

170 As expected, the release of calcein from liposomes endocytosed by cells is inhibited

171 id residues 114 to 135 of NSP4 also released calcein from liposomes.

172 , as evidenced by the concomitant release of calcein from mitochondria.

173 the release kinetics of the fluorescent dye calcein from target cells (>50 lytic events may be teste

174 cations, including removal of unencapsulated calcein from vesicles, remote loading and vesicle micros

175 ease of a charged water-soluble fluorophore, calcein, from liposomes suspended in buffer or cell cult

176 tracking the movement of the fluorescent dye calcein; (ii) immunostaining for connexin 43 (Cx43); and

177 ura-2 and differential interference contrast/calcein imaging.

178 resulted in the accumulation of fluorescent calcein in both the Golgi and the mitochondria.

179 D(o)/D for the small solute calcein in different regions of brain was in the range 3

180 eaching, adapted to examine the diffusion of calcein in inner ear explants, revealed asymmetric commu

181 MP-FPR is demonstrated on calcein in RBL-2H3 cells, using an anomalous subdiffusio

182 l) in the membrane and a fluorescent solute (calcein) in the aqueous space.

183 The fluorescent marker (calcein) incorporated into liposomes was released when t

184 vivo inhibited bone formation as measured by calcein incorporation into long bones.

185 n was assessed by micro-computed tomography, calcein injection, and osteopontin expression.

186 Entry of calcein into mitochondria after MHX indicated MPT onset.

187 MPT, as evidenced by permeation of cytosolic calcein into mitochondria and loss of the mitochondrial

188 a particle loads an anionic fluorescent dye (calcein) into the particle to a concentration exceeding

189 er, the ability of such liposomes to release calcein intracellularly, measured by a novel flow cytome

190 a reduced pH within endosomal compartments, calcein is effectively released.

191 However, quantitative analysis shows that calcein is released into the space above the bilayer (ve

192 ed in particles, whereas the calcium-binding calcein label is mainly excluded from the endoderm and i

193 l cells specifically direct the adherence of calcein-labeled platelets.

194 Calcein-labeled T cells were used to assay HIF adhesion

195 Calcein labeling of calvarial surfaces was increased in

196 Likewise, calcein labeling revealed that early bone formation was

197 culated by identifying newly formed bone via calcein labeling.

198 Using a calcein leakage assay and cryo-TEM, fusion of CP liposom

199 +/- 0.2 seconds (P(f)(mem) = 0.045 cm/s) in calcein-loaded corneal epithelial cells of wild-type mic

200 s) using fluorescence confocal microscopy on calcein-loaded RBCs.

201 e lifetime-based vesicle leakage assay using calcein-loaded vesicles.

202 Subcellular calcein localization revealed inhibition of the mitochon

203 The uptake of two fluorophores, calcein (molecular weight: 622) and fluorescein isothioc

204 Fluctuating mitochondria did not lose calcein, nor was there any effect of cyclosporin A on De

205 Folate-tethered liposomes containing calcein or doxorubicin were prepared using pteroyl-gamma

206 lentoid transfer of fluorescent dyes, either calcein or Lucifer yellow, over a time course of up to 4

207 de folated eLiposomes carrying a model drug (calcein) or a model GFP plasmid to examine the effects o

208 elator to estimate labile cytoslic Fe2+, and calcein plus an Fe3+ chelator to estimate total cytosoli

209 Calcein-positive cells were visible in all TM layers, bu

210 tissues showed PI staining in the absence of Calcein-positive cells.

211 ease in the rate and amplitude of release of calcein, possibly due to a decreased rate of flux throug

212 oxamine (1 mM) prevented bafilomycin-induced calcein quenching, indicating that bafilomycin induced r

213 the magnitude and time course of Hst-induced calcein release from C. albicans cells further showed th

214 eramide channel, we have used here assays of calcein release from liposomes.

215 mbrane capacitance, rise in conductance, and calcein release from liposomes.

216 on macroscopic electrical conductance, or on calcein release from liposomes.

217 ration of MGDG in the liposome, with maximum calcein release occurring in 20 mol % MGDG liposomes.

218 Calcein release was enhanced during apoptosis.

219 sted simultaneously); estimate end points of calcein release within 16 min of initial E:T cell contac

220 The gradual phenomenon of calcein release would be due to a competition between tw

221 control peptides promoted significantly less calcein release.

222 Through hemolysis and calcein releasing assays, it is revealed that mixtures o

223 hodamine methylester (TMRM) and quenching of calcein, respectively.

224 e the fraction of cells exhibiting uptake of calcein showed a maximum at an intermediate energy dose.

225 ring calcium uptake with the fluorescent dye calcein shows that calcium ions first penetrate the embr

226 Calcein AM, the cell-permeable derivative of calcein, shows significant antitumour activity in a wide

227 Osmotic water permeability was measured in calcein-stained epithelial cells in intact lenses from f

228 Membrane water permeabilities (P(f)(mem)) of calcein-stained surface epithelial cells were measured f

229 To determine whether calcein staining could also be used to detect abnormal b

230 ults clearly demonstrated the sensitivity of calcein staining for visualizing bone structures in deve

231 red with Alcian blue staining, we found that calcein staining indeed labels calcified skeletal struct

232 used no further increase in the already high calcein staining of Col1a1(r/r) bones.

233 X-ray, microCT, alizarin red/alcian blue and calcein staining revealed severe skeletal deformity, pre

234 Calcein staining showed that JTR-009 did not indirectly

235 ic parathyroid hormone for 30 days increased calcein-surface labeling in wild-type but caused no furt

236 e using the 'thinness ratio' and the 'cobalt-calcein' technique.

237 vely charged dyes such as Lucifer yellow and calcein than are Cx45 pores.

238 focal microscopy showed that, in the case of calcein, there was a uniform fluorescence throughout the

239 ture on the flux of the fluorescent molecule calcein through the open channel have been studied.

240 ated by staining with ethidium homodimer and calcein to discriminate live from dead cells.

241 The assay implements calcein to facilitate simple visual readout of positive

242 TAM enhances membrane permeability, inducing calcein to translocate from the interior to the exterior

243 xpressing strain specifically in the case of calcein transfer between vegetative cells and heterocyst

244 of the mutants showed enhanced lipid mixing, calcein transfer, and syncytium formation even in the pr

245 These results support an association between calcein transfer, SepJ-related septal junctions, and sep

246 Diffusive coupling (calcein transmission) in vitro was strong between Colo35

247 P1 at the plasma membrane and did not export calcein under basal or apoptotic conditions, indicating

248 amined cell viability and cellular uptake of calcein using 3T3 mouse cell suspension as a model syste

249 Cell to cell diffusion of calcein was poor among Cx43-deficient osteoblasts, whose

250 g a concentration-dependent quenching probe (calcein), we determined that MAX-induced leakage of lipo

251 photobleaching, we observed that DsRed1 and calcein were highly mobile within the matrix of individu

252 iac myocytes loaded with the fluorescent dye calcein were optically sectioned to produce a series of

253 tic pressure difference; rates of release of calcein were very slow in the absence of anionic lipid b

254 gated the use of the fluorescent chromophore calcein, which binds specifically to calcified skeletal