ライフサイエンスコーパス: annexin

1 n and dysferlin-interacting proteins such as annexins.

2 AC5, adding a new facet to the functions of annexins.

3 in diseased tissues that restrict the use of annexins.

4 dicated that CERK1 physically interacts with ANNEXIN 1 (ANN1), which was reported to form a calcium-p

5 tase 5 (PP5), formyl peptide receptor 2, and annexin 1.

6 amed tissues and concomitantly downregulated annexin-1 and IL-10 production.

7 larly, the cell type-dependent enrichment of annexins 2, 5 or 6 in calcifying EVs posits one of sever

8 tion pathway, including plasminogen receptor annexin 2A as well as downregulation of plasminogen acti

9 o experiments have identified involvement of Annexin A1 (Anx A1) in both these fusion processes.

10 ncy was associated with an early increase of annexin A1 (AnxA1) and did not modify the course of neut

11 upled with increased expression of mRNAs for annexin A1 (AnxA1) and the formyl peptide receptors [(Fp

12 scle injury and repair, herein we identified annexin A1 (AnxA1) as the extracellular trigger of macro

13 tide receptor-1 (FPR1), which interacts with Annexin A1 (ANXA1) from dead cells.

14 Annexin A1 (AnxA1) is a glucocorticoid-regulated protein

15 Annexin A1 (AnxA1) is a glucocorticoid-regulated protein

16 Annexin A1 (ANXA1) is a protein induced by glucocorticoi

17 Annexin A1 (AnxA1) is a protein involved in modulation a

18 The widely-expressed Ca(2+)-binding protein annexin A1 (ANXA1) is present in the nuclear envelope lu

19 In this work, we demonstrate that endogenous annexin A1 (ANXA1) is released as a component of extrace

20 th reperfusion was performed in wild-type or annexin A1 (AnxA1) knockout (AnxA1(-/-)) mice.

21 Annexin A1 (AnxA1) mainly acts through Formyl Peptide Re

22 We demonstrated high expression of annexin A1 (ANXA1) mRNA by MSCs and confirmed expression

23 mmatory pathway glucocorticoid receptor (GR)-annexin A1 (ANXA1) occurs.

24 tes the potential therapeutic treatment with annexin A1 (AnxA1) to induce cardiac repair after MI.

25 Annexin A1 (ANXA1), an inflammation modulator, is a pote

26 ALX/FPR2, which is activated by the protein annexin A1 (ANXA1), found in high abundance in inflammat

27 we show that these contacts are tethered by annexin A1 and its Ca(2+)-dependent ligand, S100A11, and

28 We identify annexin A1 as a specific marker for microvesicles that a

29 Mechanistically, we identify annexin A1 as an endogenous inhibitor of integrin activa

30 Deletion of FPR2 or its ligand annexin A1 enhances atherosclerotic lesion formation, ar

31 Specifically, the annexin A1 fragment Ac2-26 counteracts conformational ac

32 te the role of FPR2 and its resolving ligand annexin A1 in atherogenesis.

33 nd treatment with FPR agonists: AnxA1Ac2-26 [Annexin A1 mimetic peptide (Ac-AMVSEFLKQAWFIENEEQEYVQTVK

34 tial of 2 proresolving endogenous mediators, annexin A1 N-terminal derived peptide (AnxA1Ac2-26) and

35 comprises a small bioactive peptide from the annexin A1 protein grafted into a sunflower trypsin inhi

36 ribution of FPR2 and its proresolving ligand annexin A1 to atherosclerotic lesion formation is largel

37 f these lipids as well as by peptides (e.g., annexin A1), has been shown to be one of the receptors i

38 ulation were associated with the cleavage of annexin A1, a powerful anti-inflammatory protein known t

39 Subcellular patterning is evident as annexin A1, dysferlin, diacylglycerol, active Rho, and a

40 activated by IAV, which harbors its ligand, annexin A1, in its envelope.

41 Instructing the annexin A1-FPR2 axis harbors a novel approach to target

42 Annexin A1-regulated contacts function in the transfer o

43 d override the prosurvival effect of LPS via annexin A1.

44 proresolving mediators and proteins, such as annexin A1.

45 trophin-glycoprotein complex of proteins and annexin A1.

46 ctinin-1, moesin, 14-3-3 protein zeta/delta, annexin A1/A3/A4/A5/A6, clathrin heavy chain 1, glyceral

47 emmal repair through increased expression of annexins A1 and A6, which mediate myofiber repair.

48 Within seconds of membrane disruption, annexins A1, A2, A5, and A6 formed a tight repair "cap."

49 Endogenous anti-inflammatory annexin-A1 (ANX-A1) plays an important role in preservin

50 ed proximity labeling proteomics reveal that annexin A11 (ANXA11), an RNA granule-associated phosphoi

51 itchhike' on LAMP1-positive organelles using annexin A11 as a tether.

52 aging, we report that the intestine-specific annexin A13 (ANX A13) localizes to the tips of intestina

53 , we show that similar to dysferlin, lack of annexin A2 (AnxA2) also results in poor myofiber repair

54 1R phosphorylated the prometastatic molecule Annexin A2 (AnxA2) at Y23 and Y333 in response to stroma

55 We recently found that annexin A2 (ANXA2) co-localizes with PS-ASOs in late end

56 eport that the phospholipid-binding protein, annexin A2 (ANXA2) functions to maintain vascular integr

57 Here we reveal a role for annexin A2 (AnxA2) in host defense against infection as

58 Progressive accumulation of Annexin A2 (AnxA2) in the myofiber matrix causes FAP dif

59 -206 directly targets the oncogenes KRAS and annexin a2 (ANXA2), thereby acting as tumor suppressor i

60 n the membrane phospholipid binding protein, annexin A2 (ANXA2), we observed a significant decrease i

61 We also identify the S100A10 subunit of the annexin A2 (AnxA2)-S100A10 protein complex as a novel Mu

62 ared dye selectively binds to phosphorylated Annexin A2 (pANXA2), with high affinity at high levels o

63 Consistently, annexin A2 and a cell-internalizing, penetratin-fused ve

64 whereas the anti-inflammatory proteins (e.g. Annexin A2 and Annexin A6) were significantly upregulate

65 an anti-inflammatory tick protein, binds to annexin A2 and impairs the formation of the NLRC4 inflam

66 gnized functional link between intracellular annexin A2 and tumor cell adhesion, migration and in viv

67 tif that binds to and inhibits intracellular annexin A2 as a candidate therapeutic lead for potential

68 omatography-mass spectrometry, we identified annexin A2 as a factor H binding partner.

69 , we identified the calcium-effector protein annexin A2 as a novel binding partner for ICAM-1.

70 Here, we identify Annexin A2 as an autophagy modulator that regulates auto

71 We thus propose membrane exposure of annexin A2 as an oxidative stress signal for some Vdelta

72 Annexin A2 can contribute to AP-mediated tissue inflamma

73 graphy showed that cortical actin bundled by annexin A2 connected docked secretory granules to the pl

74 that the membrane curvature-inducing protein annexin A2 contributes to the formation of these vesicle

75 This process is dependent on the Annexin A2 effectors ARP2 and Spire1.

76 Annexin A2 expression increases after starvation in cell

77 t starvation-induced autophagy by regulating Annexin A2 expression levels.

78 nt GroEL protein in PBMCs, and knocking down annexin A2 expression resulted in significantly reduced

79 Moreover, annexin A2 expression was significantly induced by a rec

80 Annexin A2 facilitates the binding of Vamp8 to the autop

81 rinsic actin-bundling activity of endogenous annexin A2 had the opposite effects.

82 through a recently identified receptor, the annexin A2 heterotetramer (A2t).

83 Recombinant annexin A2 impaired complement regulation by factor H an

84 her demonstrated that GroEL colocolized with annexin A2 in HEK293T cells and PBMCs.

85 er, our analyses highlight the importance of annexin A2 in vesiculation of a population of Atg16L-pos

86 mococcal otitis media, the administration of annexin A2 increased AP-mediated bacterial opsonization

87 ICAM-1 clustering promotes the ICAM-1-annexin A2 interaction and induces translocation of ICAM

88 Annexin A2 knockdown abrogates starvation-induced autoph

89 In conclusion, our data show that annexin A2 limits neutrophil transendothelial migration

90 reveal that dysfunction of the BLOC-1-KIF13A-Annexin A2 molecular network underlies the pathophysiolo

91 When an annexin A2 mutant with impaired actin filament-bundling

92 S TX binds to human surfactant protein A and annexin A2 on airway epithelial cells and is internalize

93 upled with mass spectrometry identified that annexin A2 possibly interacted with GroEL protein.

94 n turn, enhances the trans-activation of the Annexin A2 promoter.

95 To understand how annexin A2 promotes this membrane remodeling, the involv

96 Absence of annexin A2 reduces both vesicle formation and homotypic

97 Further experiments showed that annexin A2 reduces the binding of factor H to cell surfa

98 sma phagocytophilum Macrophages deficient in annexin A2 secreted significantly smaller amounts of int

99 l support to our findings, better binding of annexin A2 to sialostatin L2 in sera from 21 out of 23 i

100 the cell triggers recruitment of S100A11 and Annexin A2 to the site of injury.

101 Depletion of endothelial annexin A2 using RNA interference enhances ICAM-1 membra

102 Moreover, purified annexin A2 was able to stimulate the proliferation of a

103 ication and mass spectrometry, intracellular annexin A2 was identified as the corresponding binding p

104 entify antigenic ligands of gammadelta TCRs, annexin A2 was identified as the direct ligand of Vgamma

105 In conclusion, the local production of annexin A2 within tissues suppresses regulation of the A

106 Annexin A2, a calcium-, actin-, and lipid-binding protei

107 apoptosis in host cells by interacting with annexin A2, a novel virulence mechanism in Mycoplasma ga

108 confirmed that GroEL proteins could bind to annexin A2, and confocal analysis further demonstrated t

109 Notably, caveolin-1, caveolin-2, and annexin A2, which are proteins associated with lipid raf

110 ut not nonphosphorylated PS1, interacts with Annexin A2, which, in turn, interacts with the lysosomal

111 Accordingly, Annexin a2-deficient mice were more susceptible to A. ph

112 Lipidomic analysis of annexin A2-deficient mouse cells indicates that this pro

113 Thus, annexin A2-induced actin bundling is apparently essentia

114 hat 30% of Atg16L-positive vesicles are also annexin A2-positive.

115 peripheral blood mononuclear cells and other annexin A2-specific Vdelta2(neg) gammadelta T-cell clone

116 endosomal tubules along microtubules to the Annexin A2/actin-dependent stabilization and detachment

117 enesis, and the phospholipid-binding protein annexin A3 (AnxA3), a negative regulator of adipocyte di

118 Annexin A3 colocalized with cathepsin B and C, claudin-1

119 t staining for cathepsin B, cathepsin C, and annexin A3 in cFSGS was significantly greater than in ot

120 Annexin A4 (AnxA4), a Ca(2+)- and phospholipid-binding p

121 Annexin A5 (AnxA5) binds with high affinity to PS extern

122 The phospholipid- and Ca(2+)-binding protein annexin A5 (ANXA5) is the most abundant membrane-associa

123 Annexin A5 addition to choroid plexus cell cultures rest

124 er, we validated that two of these proteins, annexin A5 and phosphoglycerate kinase 1, can bind direc

125 Similarly, annexin A5 and phospholipase A2 blocked >95% of myosin-s

126 Annexin A5 blocked platelet internalization and HepG2 pr

127 Annexin A5 blocks immunosuppressive apoptosis and promot

128 Annexin A5 depletion by siRNA led to decreased annexin A

129 cell cultures from rats were used to analyse annexin A5 effects on Abeta-induced cytotoxicity.

130 he intratumoral burst release of the protein annexin A5 from intravenously injected hollow mesoporous

131 id plexus exhibited progressive reduction of annexin A5 levels along with progressive increased Abeta

132 o analyse Abeta accumulation, cell death and annexin A5 levels compared with control subjects.

133 res, Abeta administration reduced endogenous annexin A5 levels in a time-course dependent manner and

134 On the other hand, annexin A5 levels in CSF from patients were found progre

135 ependent manner and simultaneously increased annexin A5 levels in extracellular medium.

136 Our study suggests that annexin A5 may have therapeutic potential in the treatme

137 Here, we investigated the effects of annexin A5 on Abeta toxicity in choroid plexus.

138 ge established tumours, the burst release of annexin A5 owing to diselenide-bond cleavage under the o

139 Annexin A5 siRNA also increased cell viability compared

140 nexin A5 depletion by siRNA led to decreased annexin A5 translocation into mitochondria and significa

141 Moreover, expression of annexin A5 was induced by other nephrotoxicants such as

142 We propose that annexin A5 would exert a protective role in choroid plex

143 One of these proteins, annexin A5, was previously demonstrated implicated in bl

144 tablished that autoantibodies to troponin I, annexin-A5, and beta 1-adrenegic receptor best discrimin

145 cavenging hemopexin and by the PS antagonist annexin-a5, in vitro and in vivo.

146 Earlier studies implicated annexin A6 (AnxA6) to inhibit secretion and participate

147 Chemotherapy-elicited EVs are enriched in annexin A6 (ANXA6), a Ca(2+)-dependent protein that prom

148 +) -dependent phospholipid binding annexins, Annexin A6 (AnxA6), regulates membrane trafficking along

149 Recently, we found that the depletion of annexin A6 (ANXA6), which is most abundant in the liver

150 and accumulation of phosphatidylserine (PS), annexin A6 and matrix metalloproteinase-2, which convert

151 ated Ca2+ release during membrane repair and annexin A6 as a therapeutic target to enhance membrane r

152 29) myofibers, and impaired translocation of annexin A6 associated with impaired resealing of the sar

153 tin was recruited to the site of damage, and annexin A6 cap formation was both actin dependent and Ca

154 Annexin A6 forms the repair cap over the site of membran

155 Moreover, administration of recombinant annexin A6 in a model of muscular dystrophy reduced seru

156 Annexin A6 overexpression reduced membrane injury, consi

157 Treatment with recombinant annexin A6 protected against acute muscle injury in vitr

158 and increased the production of a truncated annexin A6 protein.

159 splayed reduced translocation of full-length annexin A6 to the site of laser-induced sarcolemmal disr

160 +-binding proteins implicated in repair, and annexin A6 was previously identified as a genetic modifi

161 lustrated by literature evidence with Anxa6 (annexin a6) as an example.

162 i-inflammatory proteins (e.g. Annexin A2 and Annexin A6) were significantly upregulated by PgLPS1435/

163 nd RNA sequencing identified Anxa6, encoding annexin A6, as a modifier gene.

164 ontrast, ANXA6N32 dramatically disrupted the annexin A6-rich cap and the associated repair zone, perm

165 gnature and identified a contribution of the annexin A6/LDL receptor-related protein 1/thrombospondin

166 xon in the membrane-binding tumor suppressor annexin A7 (ANXA7) diminishes endosomal targeting of the

167 Our results reveal a novel function of annexin A7 - enabling plasma membrane repair by regulati

168 membrane and Ca(2+) flux into the cytoplasm, annexin A7 forms a complex with apoptosis linked gene-2

169 he Ca(2+) - and phospholipid-binding protein annexin A7 is part of the plasma membrane repair respons

170 Annexin A8 (AnxA8), a calcium-dependent phospholipid-bin

171 glucocorticoid response elements upstream of annexins and was reinforced by the expression of forkhea

172 and (ii) reduced glutathione S-transferase, annexin, and dermatopontin, after antigen challenge.

173 We find that biochemically identical annexins (annexin V) display different effective Ca(2+)

174 f the Ca(2+) -dependent phospholipid binding annexins, Annexin A6 (AnxA6), regulates membrane traffic

175 In this article, we show that the annexin (Anx) family members AnxA5 and AnxA13 translocat

176 Annexins are a family of membrane-associated Ca2+-bindin

177 Annexins are a family of proteins that bind to phospholi

178 Annexins are abundant cytoplasmic proteins that can bind

179 Annexins are abundant cytoplasmic proteins, which bind t

180 These data identify annexins as mediators of membrane-associated Ca2+ releas

181 Propidium iodide/annexin assays and caspase 3, caspase 7, and PARP-1 anal

182 can be used to repeatedly induce and disrupt annexin assemblies and study their structure, dynamics a

183 ion shell of the peripheral membrane protein annexin B12 were studied using MD simulations and Overha

184 polarity-sensitive annexin-based biosensor (annexin B12-Cys101,Cys260-N,N'-dimethyl-N-(iodoacetyl)-N

185 Furthermore, we show that Annexin B9, a member of a class of proteins associated w

186 ld(S) rat retinas using a polarity-sensitive annexin-based biosensor (annexin B12-Cys101,Cys260-N,N'-

187 to solid supported membranes containing the annexin binding lipids phosphatidylinositol-4,5-bisphosp

188 ylserine-binding proteins, which, along with annexin-binding protein S100A4, regulated fusogenic acti

189 In particular, EV-associated annexin calcium channelling proteins, which form a nucle

190 ow annexins facilitate repair, we visualized annexin cap formation during injury.

191 We found that annexin cap size positively correlated with increasing C

192 -dependent, membrane-binding proteins of the annexin class can reduce deleterious effects of isobutan

193 To elucidate how annexins facilitate repair, we visualized annexin cap fo

194 yclophilin, inducible nitric oxide synthase, annexins, galectin, cathepsins and heat shock proteins),

195 ens provided comparable benefits in terms of annexin gene expression and muscle repair.

196 Although seven other annexin genes are expressed in mouse utricles, mass spec

197 Annexins have been proposed to mediate Ca(2+)-dependent

198 ces the selective loss of p11 (also known as annexin II light chain, S100A10), a multifunctional prot

199 t in 5' untranslated region (5'UTR) of human Annexin II receptor (AXIIR) mRNA, there are two upstream

200 of the crystal adhesion molecules, CD44 and annexin II, in tubular epithelial cells in vitro and in

201 approaches demonstrated that three proteins, annexin II/p36, stratifin/14-3-3 sigma, and heat shock p

202 Therefore, expression of annexins in industrial strains of yeast or bacteria may

203 However, the mechanistic action of annexins in membrane repair remains largely unknown.

204 We also show that annexin is membrane-recruited and forms stable supramole

205 itope identification, we constructed an anti-annexin IV single-chain antibody (scFv) and an scFv link

206 Annexins mediate lipid raft-dependent trafficking of tra

207 entry of extracellular Ca(2+) activates the annexin membrane-binding ability, subsequently initiatin

208 We also found that annexin overexpression promoted external blebs enriched

209 An annexin peptide (Ax) served as the target.

210 Fusion also depended on extracellular annexins, phosphatidylserine-binding proteins, which, al

211 cell proliferation (cell counts), survival (Annexin-PI), viability (WST-1) and significantly reduced

212 Apoptosis was confirmed (annexin-PI, SubG1/cell-cycle, apoptotic genes, caspase-3

213 6) in lung epithelial cells, as measured by annexin/propidium iodide detection by flow cytometry.

214 s that a cotton phosphatase GhDsPTP3a and an annexin protein GhANN8b interact and reversely modulate

215 ed that GhDsPTP3a interacts with GhANN8b, an annexin protein, which plays a positive role in regulati

216 Annexin proteins function as Ca(2+)-dependent regulators

217 Thus, Annexin proteins may link membrane resealing to cytoskel

218 s in cellular morphology, high percentage of annexin-stained cells and sub-G1 populations as well as

219 ly occludes the membrane-binding surfaces of annexin, suggesting that dimerization may function as a

220 rmal in vitro apoptosis function, with lower annexin, than patients with suspected ALPS (P = .002) an

221 layed by Ca(2+) in the reversible binding of annexin to the membrane surface.

222 for EVs in eggshell mineralization, in which annexins transfer calcium into vesicles and carbonic anh

223 Tnfr1 significantly reduced tubular CD44 and annexin two expression, as well as inflammation, thereby

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

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

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

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

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

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

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

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

232 An annexin V assay used to measure eosinophil apoptosis sho

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

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

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

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

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

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

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

240 roteomic profiling, immunohistochemistry and annexin V FACS staining.

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

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

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

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

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

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

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

248 </=0.01) increase of early apoptotic cells (annexin V positive) and late apoptosis (caspase 3 activi

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

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

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

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

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

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

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

256 Annexin V staining showed no difference in apoptosis bet

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

284 oexpressed the cell surface apoptosis marker annexin V.

285 pregnancy outcomes due to interactions with annexin V.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

301 g ras-related small GTPase 10, 73% decrease; annexin VII, 8.8-fold increase; ubiquitin C-terminal hyd