ライフサイエンスコーパス: annexin V

1 e (PS) in apoptosis and blood clotting using annexin V.

2 mulated T cells, an interaction inhibited by Annexin V.

3 pendent expression of surface P-selectin and annexin V.

4 have been performed with 1 of these agents, annexin V.

5 lagen interacted with cell surface-expressed annexin V.

6 g-positive cells and by increased binding of Annexin V.

7 ction is described here between deltaPKC and annexin V.

8 motactic peptide-1, and apoptosis with 99mTc annexin V.

9 oexpressed the cell surface apoptosis marker annexin V.

10 ase promastigotes in which PS was blocked by annexin V.

11 tected by in vivo imaging with (99m)Tc-HYNIC annexin V.

12 rs (CD9 and TSG101) and contained S100A9 and annexin V.

13 The annexin V-128 protein, labeled at a single specific site

14 Comparison of (99m)Tc-annexin V-128 with (99m)Tc-HYNIC-annexin V showed that t

15 ded to the N-terminus of annexin V to create annexin V-128.

16 18F-Annexin V (14.8-51.8 MBq) was administered intravenously

17 emission computed tomography and ex vivo by annexin V/7-amino actinomycin D flow cytometry, terminal

18 donors were used to study apoptosis by using annexin V/7-aminoactinomycin D staining.

19 tion were measured by trypan blue exclusion, annexin-V/7-Aminoactinomycin D staining, and uptake of [

20 Hoescht and Annexin V/7AAD staining confirmed cell death through apo

21 n a dose-dependent manner as demonstrated by Annexin-V/7AAD staining.

22 domain of TF (called soluble TF or sTF) and annexin V, a human PS-binding protein.

23 e describe the most used method for labeling annexin V, a protein with a high affinity for apoptotic

24 The calcium-dependent protein Annexin V (A5) binds PS with high affinity, and biochemi

25 interactions of annexin V/beta5 integrin and annexin V/active PKCalpha play a role in the regulation

26 high) T(EM) cells have reduced expression of Annexin V after TCR stimulation.

27 n also resulted in a significant decrease in annexin V, an early marker of apoptosis.

28 now explore the feasibility of using (99m)Tc-annexin V, an in vivo marker of apoptosis, with SPECT to

29 99m)Tc-hydrazinonicotinamide ((99m)Tc-HYNIC) annexin V and (201)Tl and underwent dual-isotope SPECT/C

30 is in bronchoalveolar lavage was assessed by annexin V and 7-aminoactinomycin D staining.

31 Flow cytometry for annexin V and activated caspase-3 indicated that PDC are

32 Apoptosis was measured in annexin V and caspase 3 assays.

33 cell death levels (P < 0.05) as analyzed by annexin V and caspase 3/7 activity.

34 ized gld mice exhibit enhanced expression of Annexin V and caspase 3/7 indicating that FasL is import

35 D49a(+) CD8 cells had reduced proportions of annexin V and caspase 8, and >80% expressed the TNF-alph

36 radionuclide tracers, including radiolabeled annexin V and caspase inhibitors for PET and SPECT, are

37 d apoptosis of the leukocytes as measured by annexin V and CD45 staining.

38 escence staining with propidium iodide, anti-Annexin V and DAPI.

39 itions, that a transient interaction between annexin V and deltaPKC occurs in cells after deltaPKC st

40 monocyte-derived thrombin markedly increases Annexin V and factor Xa binding to platelets, consistent

41 Apoptosis and necrosis were assessed using Annexin V and flow cytometry.

42 Apoptosis was quantified by staining for annexin V and measurement of caspase 3 activity.

43 rted by high levels of the apoptosis markers annexin V and p53 in knockout testes.

44 h was predominantly necrotic as indicated by annexin V and propidium iodide (PI) staining, absence of

45 Annexin V and Sytox Green are widely used markers to eva

46 uperoxide generation with apoptotic markers (Annexin V and Sytox Green) by both flow cytometry and co

47 rescence-activated cell sorter analysis with Annexin V and terminal deoxynucleotidyltransferase-media

48 ar cytochrome c release, caspase activation, annexin V and TUNEL labeling, and cell death.

49 indicated by morphologic analysis as well as annexin V and TUNEL staining.

50 P, activation of caspases 3/7, and increased annexin V and TUNEL staining.

51 Apoptosis was assessed by Annexin-V and immunoblot analyses.

52 Annexin-V and phalloidin staining were used to detect ap

53 tacts (HHCs) were analyzed for expression of annexin-V and propidium iodide by flow cytometry.

54 or necrotic dendritic cells was evaluated by annexin-V and propidium iodide staining.

55 The proportions of annexin-V(+) and Fas-expressing T cells were elevated in

56 loss of splenocyte numbers, and induction of annexin V+ and TUNEL+ cells within the spleen that are i

57 al and apoptosis were tested by Trypan blue, annexin V, and cleaved caspase-3 assays.

58 cell lines dramatically increased caspase-3, annexin V, and DNA fragmentation activity.

59 Bak-1, Bcl-2, Bcl-xL, lactate dehydrogenase, annexin V, and propidium iodide) nor VEGF or TGF-beta le

60 id phosphatidylserine (PS) using antibodies, annexin V, and pSIVA (polarity-sensitive indicator of vi

61 Further, annexin V (AnxV) substituted for the TIM-1 IgV domain, s

62 ing delayed-type hypersensitivity assays and Annexin V apoptosis assays respectively.

63 Viability, morphological, and Annexin V apoptosis assays showed that ABT-737 alone exh

64 e cells using MTT, (3)H-thymidine uptake and Annexin-V apoptosis assays.

65 fluorescein-tagged annexin-V labeling (FITC-annexin-V), as well as by terminal nucleotide nick-end l

66 An annexin V assay used to measure eosinophil apoptosis sho

67 tidyl transferase dUTP nick end labeling and Annexin V assays).

68 deacetylase inhibitor (HDACi), using MTS and Annexin V assays, followed by molecular studies.

69 luorescein succinimidyl ester) dilution, and Annexin V assays.

70 of lymphoid cell death using a near-infrared annexin V (AV-750).

71 ther the balance between the interactions of annexin V/beta5 integrin and annexin V/active PKCalpha p

72 tics (ENR); membrane permeabilization (PRM); annexin V binding (ANX), and cell death protease activat

73 th proteasome inhibitors exhibited augmented annexin V binding and a drop in mitochondrial transmembr

74 induction of early apoptosis markers such as annexin V binding and activation of caspase 3.

75 stress, consistent with ER stress, increased annexin V binding and caspase-3 activation, consistent w

76 in the number of cells staining positive for Annexin V binding and for the TUNEL reaction.

77 r rapid cell death, which is associated with annexin V binding and membrane pore formation, is not bl

78 Apoptosis, measured by both Annexin V binding assay and terminal deoxyribonucleotidy

79 croscopic blebs, caspase 3/7 activation, and annexin V binding at the plasma membrane).

80 how that following cell activation, deltaPKC-annexin V binding is a transient and an essential step i

81 Evidence of deltaPKC-annexin V binding is provided also by FRET and by in vit

82 by flow cytometry for caspase activation and annexin V binding or by DNA fragmentation.

83 In contrast, annexin V binding showed no differences between WAS/XLT

84 BrdU incorporation and annexin V binding studies showed systemically increased

85 X expression, along with TUNEL staining, and Annexin V binding were examined in RAW 264.7 macrophages

86 xalase I, in high glucose-induced apoptosis (annexin V binding) of human retinal pericyte (HRP).

87 ediated cell death associated with increased annexin V binding, apoptotic morphology, and cleavage of

88 as externalization of phosphatidylserine by annexin V binding, as DNA fragmentation in the TUNEL ass

89 independent assays for apoptosis induction (annexin V binding, cleavage of poly[ADP-ribose] polymera

90 e chromatin condensation, DNA fragmentation, annexin V binding, lamin disruption, caspase 8 and 3 act

91 hanges in platelets, as revealed by enhanced annexin V binding, reactive oxygen species production, a

92 Annexin V binding, the inactivation of the DNA repair en

93 ncrease in p53 reporter activity but without Annexin V binding.

94 elevated caspase 3/7 activity, and increased annexin V binding.

95 the ratio between Bcl-2 and BAX, nor reduce Annexin V binding.

96 their higher levels of CXCR4 expression and annexin V binding.

97 An Annexin-V binding assay was used to evaluate the suscept

98 Annexin V binds to membranes with very high affinity, bu

99 itu fluorescent microscopy demonstrated that annexin V bound primarily to neurons at 1 and 3 d, with

100 Furthermore, depletion of endogenous annexin V, but not annexin IV, with siRNA inhibits delta

101 Densities of C4d+ and C4d+/annexin V+ (C4d+/AVB+) microvesicles were also increased

102 Once prepared, HYNIC-annexin V can be labeled with 99mTc, a widely available

103 as determined using three apoptotic assays (Annexin V, Caspase 3, and TUNEL) indicated that: a) An i

104 Triptolide induced apoptosis (assessed by Annexin V, caspase-3, and terminal nucleotidyl transfera

105 lasma membrane, detected by proteins such as annexin V; caspase activation in the intracellular compa

106 trated increased numbers of apoptotic cells (annexin V(+)/CCR3(+) bronchoalveolar lavage and bone mar

107 evated levels of endothelial microparticles (annexin V(+)/CD41(-)/CD31(+)), including subtypes expres

108 B7-H1 KO grafts had significantly fewer annexin V(+) CD8(+) T cells, and this indicated a failur

109 The percentage of annexin V+ cells was higher in Mad2+/- than Mad2+/+c-Kit

110 B and higher percentages of early apoptotic, Annexin V+ cells were observed in PBMC co-cultured with

111 The sTF-annexin V chimera is a targeted procoagulant protein tha

112 ced expression of the early apoptosis marker annexin V compared with control subjects, which was sign

113 Dissociation of the deltaPKC-annexin V complex requires ATP and microtubule integrity

114 Instead, RO(+) GC B cells were negative for Annexin V, comprised mostly (93%) of CD77(-) centrocytes

115 ting with the signal of the apoptosis marker Annexin V-Cy3.

116 ogin, a Ca(2+)-sensor protein, to execute an annexin V-dependent externalization of matrix metallopro

117 Using annexin V-depleted neutrophils, we show that glucose tra

118 is-specific liver uptake as did all forms of annexin V derivatized randomly via amino groups.

119 Nearly all studies have been done with annexin V derivatized via amine-directed bifunctional ag

120 poptosis was assessed by fluorescein-labeled annexin V detection of phosphatidylserine externalizatio

121 The recombinant homodimer of human annexin V, diannexin, has completed a Phase II Clinical

122 Annexin III or annexin V did not bind this receptor.

123 find that biochemically identical annexins (annexin V) display different effective Ca(2+) and membra

124 Both the sTF and annexin V domains had ligand-binding activities consiste

125 EMP binding to annexin V, EMPs expressing CD144 or E-selectin, and EPCs

126 ches that contained P. aeruginosa also bound annexin V-enhanced green fluorescent protein (EGFP), a m

127 Further, there was increased annexin V expression in central memory T cells of the un

128 Time course studies of annexin V expression revealed that autoreactive T cells

129 Suppression of annexin V expression using small interfering ribonucleic

130 roteomic profiling, immunohistochemistry and annexin V FACS staining.

131 Annexin V-FITC flow cytometry was used to quantify peric

132 sis in SEB-1 sebocytes as shown by increased Annexin V-FITC staining, increased TUNEL staining, and i

133 apoptosis as determined by the percentage of Annexin V-FITC+, PI- cells and the presence of caspase-3

134 reatment decreased cell viability, increased annexin V-FITC-positive cells, and increased the proport

135 n the tumor cell line, as evidenced from the annexin V-FITC/PI assay.

136 Cell cycle analysis and Annexin V-FITC/PI binding assay showed that combination

137 Annexin V-FITC/PI staining assays confirm that the cell

138 re validated by WST-1 cytotoxicity assay and annexin V-FITC/propidium iodide (PI) staining as apoptos

139 at 400 mM H2O2 as evidenced by subG1 DNA and Annexin V flow cytometry analyses and cellular immunoflu

140 ting assays that are not quantitative (e.g., annexin V flow cytometry), and it is applicable to the s

141 reduce ROS-induced apoptosis, as assayed by Annexin V flow cytometry.

142 l viability and apoptosis were determined by annexin V flow cytometry.

143 cell viability, as assessed by staining with annexin V followed by flow cytometry.

144 on is incorrect by measuring the affinity of annexin V for cells in vitro by quantitative calcium tit

145 conditions, ubiquitous "caps" with increased Annexin V, FX, and FXa binding were observed, indicating

146 Although imaging with radiolabeled annexin V has been intensively investigated, it is still

147 membrane leaflet to the outer cell surface, annexin V has proven useful for detecting the earliest s

148 inogen, showed a bias for oxidation, whereas annexin V, heparanase, ERp57, kallekrein-14, serpin B6,

149 ssed using mortality, weight changes, Tc-99m annexin-V imaging, histopathology, and immunohistochemis

150 survival by a clonogenic assay; apoptosis by Annexin V immunofluorescence; gammaH2AX, Rad51, and HDAC

151 l ion beam-scanning electron microscopy with Annexin V immunogold-labeling revealed a complex organiz

152 Annexin V-immunogold staining revealed that the calcium-

153 of deltaPKC, thus identifying a new role for annexin V in PKC signaling and a new step in PKC activat

154 Further, annexin V (in the absence of Ca(2+)) or heparin outcompe

155 /P stimulation and interaction of S100A9 and annexin V indicated that a phosphatidylserine-annexin V-

156 ding to the interaction site for deltaPKC on annexin V, inhibits deltaPKC translocation and deltaPKC-

157 In this method, annexin V is first attached to the bifunctional chelator

158 The membrane-binding activity of annexin V is much more sensitive to amine-directed chemi

159 Because annexin V is up-regulated during pathological mineraliza

160 Labeled annexin V is widely used to detect cell death in vitro a

161 rate of neutrophil apoptosis, as measured by Annexin V labeling and morphological analysis.

162 on, poly(ADP-ribose) polymerase cleavage and Annexin V labeling.

163 RGC death was analyzed by fluorescein-tagged annexin-V labeling (FITC-annexin-V), as well as by termi

164 hile increasing sub-G0 DNA fragmentation and Annexin V markers of apoptosis.

165 These interactions led to a stimulation of annexin V-mediated Ca(2+) influx resulting in an increas

166 inomycin D were observed, but the absence of annexin V membrane staining supported that neutrophils d

167 New annexin V molecules labeled by site-specific methods wil

168 s, the most well-studied example being (18)F-annexin V; more recently, probes that target caspase end

169 R pathway (by adding PS blocking antibodies, annexin V, mutant MFG-E8 unable to bind VR, or VR antago

170 h were confirmed with positive control, anti-Annexin V (MV universal marker).

171 locking exposed phosphatidylserine by adding annexin V or an antibody to phosphatidylserine or inhibi

172 D36 antibody or by blockade of exposed PS by annexin V or anti-PS IgM.

173 ted by saturating MP phosphatidylserine with annexin-V, or with inhibitors of endothelial ROS product

174 te chondrocyte apoptosis, a peptide mimic of annexin V (Penetratin (Pen)-VVISYSMPD) that binds to bet

175 was assessed via caspase 3/7 activation and Annexin V/PI flow cytometry.

176 ts as measured by caspase 3/7 activation and Annexin V/PI flow cytometry.

177 lity/apoptosis was measured by MTT assay and Annexin V/PI staining , activation related genes includi

178 (LDH) release assay, Hoechst 33342 staining, annexin V/PI staining, and JC-1 staining.

179 Apoptosis was quantified by Annexin V/PI staining.

180 ion-induced apoptosis as judged by decreased annexin-V/PI staining, caspase-3 activation, and PARP cl

181 </=0.01) increase of early apoptotic cells (annexin V positive) and late apoptosis (caspase 3 activi

182 k180 in ECs reduced caspase-3/7 activity and annexin V-positive cell number upon induction of apoptos

183 ly response to rPAI-1(23) was an increase in annexin V-positive cells and phosphorylated (p) JNK isof

184 howed both apoptotic (cleaved caspase 8- and annexin V-positive) and living cells.

185 Despite an increase in the number of annexin V-positive, 7-amino-actinomycin D (7-AAD)-negati

186 t increase in apoptotic cells as revealed by Annexin V positivity as well as proteolytic processing o

187 Apoptosis-associated events, including annexin V positivity, caspase-3 activation, and cleavage

188 lenge (P < .05), higher levels of apoptosis (Annexin V positivity, P < .005), and less lung allergic

189 ith only low levels of ex vivo staining with annexin V, probably due to the rapid clearance of apopto

190 icantly higher percentages of late apoptotic Annexin V(+) propidium-idodide(+) liver-infiltrating MNC

191 optosis, which was associated with increased Annexin-V(+)/propidium iodide (PI)(-) cells, cleaved PAR

192 Annexin V, propidium iodide, and acridine orange stainin

193 LL cells is confirmed by viable cell counts, annexin V/propidium iodide and tetramethyl-rhodamine eth

194 The result of a fluorescent microscopic annexin V/propidium iodide assay, performed in microflui

195 e, as indicated by PARP-1, caspases 3/7, and annexin V/propidium iodide assays.

196 of the cancer cells has been determined via Annexin V/Propidium iodide stain and flow cytometry.

197 lling was primarily necrotic as judged using Annexin V/propidium iodide staining.

198 ne, doxorubicin, or H2O2 and was measured by annexin V/propidium iodide staining.

199 ated from the CNS showed significantly fewer annexin V/propidium iodide-positive lymphocytes in the C

200 Several assays, including Western blotting, annexin-V/propidium iodide binding, comet, and micronucl

201 included cellular viability (calcein AM and annexin-V/propidium iodide), reactive oxygen species (RO

202 Instead, a high frequency of annexin V-reactive CD8alpha(+) dendritic cells (DCs), wh

203 usion, the interactions between collagen and annexin V regulate mineralization of growth plate cartil

204 ted dishes, or overexpression of full-length annexin V) resulted in increase of [Ca(2+)](i), alkaline

205 Flow cytometry using Annexin V revealed that cell death was by apoptosis.

206 nnexin V indicated that a phosphatidylserine-annexin V-S100A9 membrane complex facilitates hydroxyapa

207 A secreted Annexin V (sAnxV::GFP) PS sensor reveals that exPS appea

208 of (99m)Tc-annexin V-128 with (99m)Tc-HYNIC-annexin V showed that the protein labeled at the endogen

209 mice assessed in vivo by technicium-labeled annexin V single photon emission computed tomography and

210 ll sorting analysis of propidium iodide- and annexin V-stained transfected cells, immunoblot analysis

211 tumor cells, which was confirmed by positive Annexin V staining and an increase of poly(ADP-ribose) p

212 ed apoptosis in cancer cells as indicated by Annexin V staining and caspase activation.

213 thdrawal-induced apoptosis, as determined by Annexin V staining and caspase cleavage, and this was as

214 Apoptosis was measured by Annexin V staining and caspase-3 enzymatic activity assa

215 ervical cancer cells as measured by enhanced Annexin V staining and cleavage in PARP protein.

216 ion and apoptotic cell death as evidenced by annexin V staining and DNA fragmentation (TUNEL) assays.

217 tion of programmed cell death as assessed by Annexin V staining and DNA fragmentation assays.

218 Annexin V staining and flow cytometry were used to deter

219 cycle arrest and apoptosis as determined by Annexin V staining and increased cleaved caspase3 and Ba

220 R-K10a showed less induction of apoptosis by annexin V staining and terminal deoxynucleotidyltransfer

221 GW0742 and RA increased annexin V staining as quantitatively determined by flow

222 s as assessed by caspase-3 activation assay, Annexin V staining assay, or by visual analysis for the

223 ignificantly decreased apoptosis measured by annexin V staining but did not affect expression of Bcl2

224 In contrast, annexin V staining did not reveal increased apoptosis, a

225 inucleotide (NAD) induce a rapid increase of annexin V staining in NKT cells in vitro, a response tha

226 increased Bim expression in melanocytes, and Annexin V staining indicated that detachment induced cel

227 Annexin V staining indicates increased apoptosis of Tmod

228 ne and DNA degradation but do not ablate the annexin V staining or the induction of apoptosis by Clas

229 sfected COS-1 cells expressing P450 2C2, and annexin V staining was consistent with the activation of

230 ession, and apoptosis (DNA fragmentation and annexin V staining) in vitro using A549 cells and primar

231 (immunoblotting); and eventually apoptosis (annexin V staining) than did either drug alone.

232 (by trypan blue staining), and apoptosis (by annexin V staining), and we used caffeine and small inte

233 amindino-2-phenylindole dihydrochloride) and Annexin V staining, along with activated Caspases 3 and

234 ed apoptosis as indicated by cell viability, Annexin V staining, and caspase activation.

235 ptosis as indicated by caspase-3 activation, annexin V staining, and characteristic changes in cellul

236 RAW264.7 cells exhibited cytopathic effects, annexin V staining, and cleaved caspase 3.

237 el of apoptosis assessed by pycnotic nuclei, annexin V staining, and PARP cleavage.

238 trated by cytochrome c translocation, TUNEL, annexin V staining, and preservation of mitochondrial me

239 ned by poly(ADP-ribose) polymerase cleavage, Annexin V staining, and terminal deoxynucleotidyl transf

240 able to increase cAMP, reduce ATP and elicit annexin V staining, but the decrease in ATP and the anne

241 (EC(50) approximately 50 nM), as measured by annexin V staining, caspase 3 activity, cleavage of poly

242 nism to apoptosis, as evidenced by increased annexin V staining, condensation of chromatin, and cleav

243 ures of apoptosis, as evidenced by increased annexin V staining, decreased DNA content, and appearanc

244 animals showed little excision but increased annexin V staining, implying that survivin is required f

245 minal kinase 3, caspase 3, and cytochrome C, Annexin V staining, RNA degradation, and oligonucleosoma

246 Combined with Annexin V staining, this genotype analysis demonstrated

247 Annexin V staining, TUNEL, and hypodiploidy showed a sub

248 retinal cells from apoptosis was assessed by annexin V staining.

249 of apoptotic CE cells, evidenced by positive annexin V staining.

250 tosis in MMC-treated cells was detected with annexin V staining.

251 ase activity, caspase activation, TUNEL, and annexin V staining.

252 robust increases in caspase 3 activation and annexin V staining.

253 ttendant increase in caspase 3 activation or annexin V staining.

254 plasma membrane, as evidenced by diminished annexin V staining.

255 tosis, as evidenced by DNA fragmentation and annexin V staining.

256 lymerase cleavage, cytochrome c release, and Annexin V staining.

257 both KBM5 and KBM5-STI571 cells as shown by annexin V staining.

258 bserved using propidium iodide exclusion and annexin V staining.

259 by cell viability assay, DNA laddering, and Annexin V staining.

260 n of apoptosis as determined by TUNEL assay, Annexin-V staining and PARP-1 cleavage in a dose-depende

261 The Annexin-V staining and Western blot analysis indicated t

262 sis for poly(ADP)ribose polymerase cleavage, annexin-V staining by flow cytometry, and/or the presenc

263 y, cell cycle analysis, propidium iodide and annexin-V staining, and caspase-3-mediated proteolytic a

264 crease in apoptotic cell death as assayed by Annexin-V staining, caspase-3 activation and PARP cleava

265 re quantified by propidium iodide uptake and annexin-V staining, respectively.

266 Finally, by FACS analysis using Annexin-V staining, we demonstrated that the H-Ras-ERK-i

267 optosis as observed by FACS analysis through Annexin-V staining.

268 optosis by caspase 9 and 3/7 activity and by annexin-V staining.

269 ght affect tumor apoptosis, as determined by annexin-V staining.

270 Ki-67 and annexin V stainings revealed a faster turnover rate and

271 l subsets were quantified by flow cytometry; annexin-V status identified apoptotic cells and phosphor

272 ine, at DMSO concentrations >1% (v/v), using annexin V, terminal deoxynucleotidyl transferase dUTP ni

273 were significantly more likely to coexpress annexin V than equivalent, Fas-negative cells, suggestin

274 overexpression of N terminus-deleted mutant annexin V that does not bind to type II collagen and sho

275 mimic lacking TIM sequences and composed of annexin V, the mucin-like domain of alpha-dystroglycan,

276 lyx damage (histone-complexed DNA fragments, annexin V, thrombomodulin, syndecan-1), platelet activat

277 These findings suggest that binding of annexin V to active PKCalpha stimulates apoptotic events

278 ity was inhibited pharmacologically by using annexin V to block phosphatydilserine residues on apopto

279 -Cys-Gly-His) was added to the N-terminus of annexin V to create annexin V-128.

280 surface markers, intracellular markers, and annexin V to detect early apoptosis.

281 In summary, binding of annexin V to membranes is driven by both enthalpic and e

282 this study, we utilized fluorescently-tagged Annexin V to observe the externalization of PS on the pl

283 as also associated with decreased binding of annexin V to platelets activated with collagen-related p

284 eutrophil apoptosis (assessed by morphology, annexin V/To-Pro3 staining, and mitochondrial membrane p

285 effects of PDI inhibition were sensitive to annexin V treatment, suggesting exposure of phosphatidyl

286 ired 95% by pretreating apoptotic cells with annexin V, underscoring the requirement for phosphatidyl

287 (99m)Tc-HYNIC annexin V uptake as percentage injected dose (x10(-4)) d

288 (99m)Tc-HYNIC annexin V uptake as percentage left ventricle by scannin

289 (99m)Tc-Annexin V uptake in injured hemispheres was significantl

290 histologically correlated with radiolabeled annexin V uptake seen by SPECT.

291 (99m)Tc-HYNIC annexin V uptake was correlated with quantitative caspas

292 myocardium, infarct size, and (99m)Tc-HYNIC annexin V uptake were quantified from the scans from day

293 Annexin V was modified with 4 different amine-directed a

294 The affinity of annexin V was the same regardless of the head group pres

295 FVIII, prothrombin, and PS-sensitive marker Annexin V were distributed nonhomogeneously: they were p

296 Annexin V, which binds to anionic phospholipids, attenua

297 We show that overexpression of annexin V, which binds to the cytoplasmic domain of beta

298 elease calcifying MVs enriched in S100A9 and annexin V, which contribute to accelerated microcalcific

299 dging virus to cells, but, surprisingly, not annexin V, which has been used to block phagocytosis of

300 pha, IL-15Rbeta, and Bcl-2, and reacted with Annexin V, which is indicative of a preapoptotic state.

301 he expression of the early apoptosis marker, annexin-V, which was prevented by Jnk and p38 inhibition