ライフサイエンスコーパス: annexin V

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

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

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

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

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

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

7 pregnancy outcomes due to interactions with annexin V.

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

9 lagen interacted with cell surface-expressed annexin V.

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

11 ction is described here between deltaPKC and annexin V.

12 that it was abolished by MP PS capping using annexin V.

13 oexpressed the cell surface apoptosis marker annexin V.

14 RP and increase in the surface expression of Annexin-V.

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

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

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

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

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

20 idly suppress the fluorophores conjugated to annexin V, a phosphatidylserine-binding probe commonly u

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

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

23 r dynamics simulations (MDSs) to analyze how annexin-V (A5) binds to phosphatidylserine (PS)-rich mem

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

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

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

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

28 99m)Tc-hydrazinonicotinamide ((99m)Tc-HYNIC) annexin V and (201)Tl and underwent dual-isotope SPECT/C

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

30 for HU and identify potential therapeutics: annexin V and anti-ICAM-1 antibodies.

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

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

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

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

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

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

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

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

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

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

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

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

43 says and flow cytometry, after staining with Annexin V and PI respectively.

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

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

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

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

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

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

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

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

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

65 An annexin V assay used to measure eosinophil apoptosis sho

66 he molecule cytotoxic, were elucidated by an annexin V assay.

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 The expression of TIM-3 and annexin V (AV) as well as the production of IFN-gamma an

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

72 nt organisms, here, by combining an improved annexin V-based CaPLSase-imaging assay with inside-out p

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

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

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

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

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

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

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

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

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

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

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

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

85 BrdU incorporation and annexin V binding studies showed systemically increased

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 We also performed annexin V cell death assays to detect apoptosis.

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

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

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

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

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

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

114 ttenuated cell death with immunostaining for annexin V, cytochrome C, and caspases 3 and 9 pointing t

115 is, which is characterized by the binding of Annexin V, demonstrates that programmed cell death can b

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

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

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

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

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

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

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

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

126 Suppression of annexin V expression using small interfering ribonucleic

127 roteomic profiling, immunohistochemistry and annexin V FACS staining.

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

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

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

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

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

133 Flow cytometry based-Annexin V-FITC/PI double-staining was used to further qu

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

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

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

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

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

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

140 for many researchers to study apoptosis are annexin V-fluorophore conjugates.

141 t autologous Gag peptide-pulsed CD4 T cells (Annexin V(+)) following in vitro stimulation were assess

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

143 trates superior performance when compared to annexin V, for both fluorescence imaging and flow cytome

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

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

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

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

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

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

150 Annexin V-immunogold staining revealed that the calcium-

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

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

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

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

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

156 Because annexin V is up-regulated during pathological mineraliza

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

158 ty MOMP was tested via comet assay, CyQuant, annexin V, JC-1, cytochrome C subcellular localization,

159 ymmetric vesicles containing PS and employed Annexin V labeled with an Alexa Fluor 568 fluorophore as

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

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

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

163 olipin from periodontitis subjects increases annexin V levels on the BeWo choriocarcinoma cell line,

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 pin from periodontitis subjects competes for annexin V on an artificial phosphatidylserine monolayer,

172 e protective 2-dimensional lattice formed by annexin V on trophoblast surfaces by anticardiolipin, vi

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

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

175 y blocking accessibility of exposed PS using Annexin V or through microglial loss of TREM2.

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

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

178 d higher levels of apoptosis, as assessed by annexin V/PI assays and increased caspase 3/7 activity i

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

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

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

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

183 d HeLa and BE(2)-C cells was demonstrated by Annexin V/PI staining.

184 Apoptosis was quantified by Annexin V/PI staining.

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

186 </=0.01) increase of early apoptotic cells (annexin V positive) and late apoptosis (caspase 3 activi

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

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

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

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

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

192 re equally effective at inducing cell death (Annexin-V positivity) of purified eosinophils from NDs a

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

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

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

196 Annexin V, propidium iodide, and acridine orange stainin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

215 strong correlations with fluorescence-based annexin V staining and can be used to study concentratio

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

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

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

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

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

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

222 Annexin V staining and flow cytometry were used to deter

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

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

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

226 e cell microscopic imaging and analysis, and annexin V staining assays were conducted.

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

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

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

230 Annexin V staining indicates increased apoptosis of Tmod

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

232 Annexin V staining showed no difference in apoptosis bet

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

249 Combined with Annexin V staining, this genotype analysis demonstrated

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

251 orescence-activated cell sorting (FACS) with annexin V staining.

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

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

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

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

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

257 ttendant increase in caspase 3 activation or 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 re quantified by propidium iodide uptake and annexin-V staining, respectively.

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

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

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

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

271 ere pre-coated with a lipid-binding protein, annexin V, suggesting externalized PS to be key in media

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

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

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

282 a cell line, consistent with mobilization of annexin V to the cell surface to facilitate repair follo

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

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

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

286 (99m)Tc-HYNIC annexin V uptake as percentage injected dose (x10(-4)) d

287 (99m)Tc-HYNIC annexin V uptake as percentage left ventricle by scannin

288 (99m)Tc-Annexin V uptake in injured hemispheres was significantl

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

290 (99m)Tc-HYNIC annexin V uptake was correlated with quantitative caspas

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

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

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

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

295 Annexin V, which binds to anionic phospholipids, attenua

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

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

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

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

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