ライフサイエンスコーパス: externalization

1 ( Wm depolarization, cytosolic Ca2+, and PS externalization).

2 ed APLT, activated scramblase, and caused PS externalization.

3 ible to the dye or antibodies, demonstrating externalization.

4 /oxidation and inhibition of APLT causing PS externalization.

5 ced S-nitrosylation, APLT inhibition, and PS externalization.

6 , caspase activation, and phosphatidylserine externalization.

7 l membrane potential, and phosphatidylserine externalization.

8 Sickle RBCs exhibit a wide range of PS externalization.

9 hrough the modulation of membrane PS residue externalization.

10 caspase-3 activation and phosphatidylserine externalization.

11 y, DNA fragmentation, and phosphatidylserine externalization.

12 ed modest (20%) inhibition of APT without PS externalization.

13 apoptosis, including phosphatidylserine (PS) externalization.

14 lysis of poly(A)DP-ribose polymerase, and PS externalization.

15 at different pHout and mechanisms of urease externalization.

16 tached to the extracellular matrix following externalization.

17 ant activity through phosphatidylserine (PS) externalization.

18 m-independent PLA(2) in lysoPC-induced TRPC6 externalization.

19 TF protein expression or phosphatidylserine externalization.

20 s the dynamics associated with VP N terminus externalization.

21 equired to support coagulation on ECs via PS externalization.

22 ) concentration, and phosphatidylserine (PS) externalization.

23 crambling leading to phosphatidylserine (PS) externalization.

24 lack of CD74 and failed in subsequent CXCR7 externalization.

25 wer nsPEF exposure parameters compared to PS externalization.

26 locity in the TIRF zone, and prevented their externalization.

27 o identify the source of Ca2+ critical to PS externalization.

28 se of Ca2+ from lysosomes is critical for PS externalization.

29 fragmentation of DNA and phosphatidyl serine externalization; activation of caspase-3, caspase-9, and

30 ques for visualization of phosphatidylserine externalization, activity of caspases, and mitochondrial

31 ditional studies assessed phosphotidylserine externalization after a 24-h exposure to taurolidine usi

32 iation and propagation of phosphatidylserine externalization after axotomy.SIGNIFICANCE STATEMENT Axo

33 enders OFF-medication, during temporary lead externalization after deep brain stimulation surgery.

34 ies of two lipid transporters involved in PS externalization, aminophospholipid translocase (APLT) an

35 nnels, allowing calcium influx that promotes externalization and activation of TRPC6 channels.

36 ffects of NO were insufficient to prevent PS externalization and apoptosis following oxidative stress

37 : by increasing TG2-cell surface trafficking/externalization and by mediating RGD-independent cell ad

38 toposide as determined by phosphatidylserine externalization and caspase activation.

39 abrogated DNA laddering, phosphatidylserine externalization and collapse of the mitochondrial transm

40 mbrane blebbing, although phosphatidylserine externalization and DNA degradation proceed, indicating

41 er cells to LL-37 induced phosphatidylserine externalization and DNA fragmentation in a manner indepe

42 TMEM16 inhibitor benzbromarone prevented PS externalization and EC procoagulant activity and protect

43 e region of the capsid is important for VP1u externalization and genome ejection, and one 5-fold vari

44 mpetitive recipient can stimulate metabolite externalization and initiate a positive-feedback loop of

45 bacteria no longer induce phosphatidylserine externalization and instead protect infected cells again

46 gether our findings indicate that annexin A1 externalization and its proteolytic processing into a ch

47 rks of apoptosis, such as phosphatidylserine externalization and loss of mitochondrial transmembrane

48 s, thus resulting in more phosphatidylserine externalization and membrane rearrangement.

49 ether high UA induce phosphatidylserine (PS) externalization and microparticle (MP) shedding in cultu

50 2O2)-induced apoptosis was accompanied by PS externalization and oxidation of different phospholipids

51 of preventing PS peroxidation, can block PS externalization and phagocytosis of apoptotic cells by m

52 We propose that phosphorylation favors CTD externalization and prompts its compaction at the capsid

53 Externalization and proteolytic processing of pro-IL-1 b

54 ed annexin V detection of phosphatidylserine externalization and quadrant analysis with flow cytometr

55 reatment with TMEM16 inhibitors prevented PS externalization and reduced fibrin formation in the vess

56 in and other proteolysis, and less efficient externalization and secretion.

57 ined by increases in phosphatidylserine (PS) externalization and sub-G1 events.

58 ely inhibited the subsequent increases in PS externalization and sub-G1 events.

59 nti-CD3/CD28) as a model for TCR-mediated PS externalization and T cell stimulation, we investigated

60 c basis for the initial steps of VP1 and VP4 externalization and uncoating.

61 on oxidative stress, caspase activation, PS externalization, and cell death suggests that this balan

62 ly mitochondrial injury, phosphatidyl serine externalization, and DNA degradation, implicating a gran

63 tial, caspase activation, phosphatidylserine externalization, and DNA fragmentation.

64 lular calcium dysregulation, prevents PtdSer externalization, and enables months-long protection of v

65 itrosative stress inhibited APLT, induced PS externalization, and enhanced recognition and eliminatio

66 aspase-3 activation, phosphatidylserine (PS) externalization, and GSH depletion.

67 ose) polymerase cleavage, phosphatidylserine externalization, and hypodiploid DNA content.

68 lymerase (PARP) cleavage, phosphatidylserine externalization, and increased accumulation of cells in

69 by morphological changes, phosphatidylserine externalization, and internucleosomal DNA fragmentation,

70 ace fibrinogen retention, phosphatidylserine externalization, and platelet procoagulant activity in a

71 The BB2r binding affinities, externalization, and protein-association properties of t

72 brane microvesiculation, phosphatidyl serine externalization, and proteolysis of procaspase-9, procas

73 n (assessed with TOPRO), phosphatidyl serine externalization (Annexin V labeling), or DNA fragmentati

74 Etoposide also inhibited PS externalization as well as phagocytosis of apoptotic cel

75 ed release of AA from EC membranes and TRPC6 externalization, as well as preserved EC migration in th

76 ndent mechanism, by increasing their rate of externalization at extrasynaptic sites.

77 related with the onset of phosphatidylserine externalization, but preceded effector procaspase proces

78 reactive oxygen species levels increase ATP externalization by monocytes, resulting in enhanced infl

79 F-68 treatment prevented phosphatidylserine externalization, caspase activation, loss of mitochondri

80 (100 microm), as shown by phosphatidylserine externalization, caspase-3 activation, development of a

81 by DNA fragmentation nor phosphatidyl serine externalization, characteristics of apoptosis.

82 er Wm depolarization, cytosolic Ca2+, and PS externalization compared with healthy controls (n = 18)

83 with thrombosis had significantly higher PS externalization compared with those without.

84 ( Wm depolarization, cytosolic Ca2+, and PS externalization) compared with healthy volunteers and se

85 osomal DNA fragmentation, phosphatidylserine externalization, cytochrome c release, and effector casp

86 line that is deficient in phosphatidylserine externalization, did not release GSH during apoptosis, a

87 lymerase degradation, and phosphatidylserine externalization, directly verified that HgCl2 attenuated

88 fmk, and Boc-Asp.fmk, blocked Fas-induced PS externalization, disruption of Deltapsim, and cell death

89 llular esterase activity, phosphatidylserine externalization, DNA strand breaks, or caspase activatio

90 ar effects, that nanoelectropulse-induced PS externalization does not require calcium in the external

91 erefore, PS oxidation is not required for PS externalization during AMVN-induced apoptosis.

92 , and recently we could show that annexin A1 externalization during secondary necrosis provides an im

93 son's disease patients during temporary lead externalization during surgery for deep brain stimulatio

94 ed in Scott syndrome, was required for PE/PS externalization during thrombin activation and energy de

95 exhibits time-dependent high rates of cable externalization exceeding 20% at >5 years of dwell time.

96 One patient with externalization exhibited new noise on near-field electr

97 It is then proposed that such externalization facilitated a broader shift to a vastly

98 is study examined the relationships among PS externalization, fetal hemoglobin content, hydration sta

99 Probit analysis results revealed that PS externalization followed the non-linear trend of (tau*ED

100 alization initiates respiratory burst and PS externalization, followed by a reduction in both the pro

101 n the VP1u region that likely facilitate its externalization from the capsid interior during infectio

102 at the group IIA phospholipase acts prior to externalization from the cells.

103 leaky, and I review mechanisms of metabolite externalization from the context of cross-feeding.

104 Phosphatidylserine (PS) externalization has been observed on the outer leaflet o

105 o participate in apoptosis, their role in PS externalization has not been established.

106 lets exhibited defects in phosphatidylserine externalization, high-level surface fibrinogen retention

107 rs of electrical lead failure included cable externalization, higher left ventricular ejection fracti

108 to study the dynamics of phosphatidylserine externalization immediately after axonal injury in purif

109 tein function and reveal that CTLA-4 protein externalization imparts suppressor function to both regu

110 t the minimum field strength required for PS externalization in actively metabolizing Jurkat cells wi

111 cleavage product, acCED-8, that promotes PS externalization in apoptotic cells and can induce ectopi

112 Consistent with its role in promoting PS externalization in apoptotic cells, ced-8 is important f

113 Viral infection can induce PS externalization in host cells, resulting in increased ou

114 led to lower negatively-charged phospholipid externalization in PDEVs, which was reflected in the low

115 Enhanced PS externalization in platelets from COVID-19 patients in t

116 These studies indicate that PS externalization in sickle cells may be low level, as obs

117 Overall, externalization in the digital age changes what people a

118 membrane phospholipid symmetrization and PS externalization in uptake of apoptotic cells by mouse ma

119 rovide evidence for the relevance of calpain externalization in vivo in regulating IL-17A expression

120 ine B, to investigate the role of PIP2 in PS externalization in whole platelets.

121 the onset and velocity of phosphatidylserine externalization in wild-type axons significantly, replic

122 ed to other cell events characterized by APL externalization, including cell division and vesiculatio

123 ced by apoptosis-specific phosphatidylserine externalization, increased caspase-3 activity, chromatin

124 regulated at several levels, including their externalization, internalization, and lateral diffusion

125 The first mode mapped onto an externalization/internalization axis and showed a strong

126 ectric fields induce phosphatidylserine (PS) externalization, intracellular calcium redistribution, a

127 Our data demonstrate that glycolytic enzyme externalization is a common and early aspect of cell dea

128 Phosphatidylserine externalization is an early molecular signature for apop

129 Phosphatidylserine externalization is associated with cellular development,

130 PS externalization is generally attributed to an increase i

131 Using a novel model system, we show that PS externalization is inducible, reversible, and independen

132 leaflet, and demonstrate phosphatidylserine externalization is rate-limiting for experience-dependen

133 While it is well established that PS externalization is regulated by activation of a calcium-

134 It explains how ALT externalization is the combined consequence of lobular-l

135 TMEM16F-dependent PS externalization is well characterized in platelets.

136 Moreover, the cellular uptake and externalization kinetics of [(225)Ac]Ac-PSMA I&T were co

137 a(...) induces pronounced phosphatidylserine externalization, membrane blebbing, and ectosome release

138 This externalization most likely is effected by cell death an

139 by nsPEF, including phosphatidylserine (PS) externalization, nanopore-conducted currents, membrane b

140 inhibitor of APLT, we showed that PS and CRT externalization occurred together in an S-nitrosothiol-d

141 APL externalization occurs in numerous events, and it is rel

142 in vivo and in vitro demonstrate that MMP-2 externalization occurs on demand and that its loss slows

143 This protocol measures externalization of aminophospholipids (APLs) to the outs

144 stage of inflammation leads to cell surface externalization of Annexin A1 (AnxA1), an effector of en

145 llular traps (NETs), which display increased externalization of bactericidal, immunostimulatory prote

146 These results indicate that ATP stimulates externalization of both IL-1 alpha and IL-1 beta.

147 termediate (135S) particle, resulting in the externalization of capsid proteins VP4 and the amino ter

148 onses to IL-31 were assessed for chemotaxis, externalization of CD63 and CD203c as well as the releas

149 cenario where inside-out abrasion results in externalization of conductor cables, with a higher risk

150 pecific insulation abrasion characterized by externalization of conductor cables.

151 In CAPS monocytes, LPS induces the externalization of copious amounts of ATP (10-fold), whi

152 r characterization of the apoptosis-specific externalization of glycolytic enzyme molecules may provi

153 Externalization of IL-1 beta required active recognition

154 r protein, to execute an annexin V-dependent externalization of matrix metalloprotease-2 (MMP-2) for

155 oth precursor and mature IL-37, but only the externalization of mature IL-37 was dependent on ATP.

156 roxy-tetraindole 8 induces apoptosis through externalization of membrane phosphatidylserine, DNA frag

157 , and results in potentiation of NCS-induced externalization of membrane PS, two events associated wi

158 ent endocytic pathway, where low pH triggers externalization of membrane-disrupting (y) peptides from

159 atory diseases have been associated with the externalization of modified autoantigens in peripheral b

160 clearance mechanisms that promote excessive externalization of modified cellular and nuclear debris

161 ology of apoptotic cell death results in the externalization of numerous autoantigens on the apoptoti

162 red exocytosis by the release of VWF and the externalization of P-selectin.

163 ng how the need to effectively advertise our externalization of particular moral commitments generate

164 nd Annexin V, the latter labeling scramblase externalization of phosphatidyl serine.

165 se Xk-related protein 8 (Xkr8) regulates the externalization of phosphatidylserine (PS) during apopto

166 Scramblase Xkr8 regulates the externalization of phosphatidylserine (PS) during apopto

167 Apoptosis is associated with the externalization of phosphatidylserine (PS) in the plasma

168 These events are followed by externalization of phosphatidylserine (PS), disruption o

169 ge recognition of apoptotic cells depends on externalization of phosphatidylserine (PS), which is nor

170 Externalization of phosphatidylserine after Ca/P stimula

171 and -9, poly(ADP-ribose) polymerase, and the externalization of phosphatidylserine after treatment of

172 C loading, some of the macrophages exhibited externalization of phosphatidylserine and DNA fragmentat

173 wild type underwent apoptosis as measured by externalization of phosphatidylserine and the display of

174 ion of apoptotic bodies, but had an enhanced externalization of phosphatidylserine at the cell surfac

175 apoptosis in SH-SY5Y cells when measured as externalization of phosphatidylserine by annexin V bindi

176 The rapid externalization of phosphatidylserine by infected cells

177 disorder caused by impaired Ca(2+)-dependent externalization of phosphatidylserine in activated plate

178 zone B cells bind rAnV, suggesting that the externalization of phosphatidylserine occurs once mature

179 ce of internucleosomal DNA fragments and the externalization of phosphatidylserine to the outer membr

180 Moreover, externalization of phosphatidylserine upon P falciparum

181 rmeability transition between 30 and 60 min, externalization of phosphatidylserine within 2 hr, and d

182 s TMEM16F lipid scramblase, facilitating the externalization of phosphatidylserine, a key "fuse-me" s

183 liest events in programmed cell death is the externalization of phosphatidylserine, a membrane phosph

184 tosis: loss of membrane asymmetry due to the externalization of phosphatidylserine, accumulation of r

185 a loss in mitochondrial membrane potential, externalization of phosphatidylserine, and DNA fragmenta

186 depolarization, followed by calcium influx, externalization of phosphatidylserine, and loss of membr

187 bited expression of apoptotic biomarkers and externalization of phosphatidylserine, and reduced phago

188 apoptosis, including chromatin condensation, externalization of phosphatidylserine, caspase activity,

189 s, including increased membrane rigidity and externalization of phosphatidylserine, consistent with e

190 dria nor the inhibition of secretion and the externalization of phosphatidylserine, indices of neutro

191 Inhibition of NF-kappa B resulted in the externalization of phosphatidylserine, induction of DNA

192 iated with a 20-40% decrease in cell volume, externalization of phosphatidylserine, loss of mitochond

193 e activity and is characterized by the rapid externalization of phosphatidylserine, nuclear condensat

194 We found that the externalization of phosphatidylserine, which can be full

195 through pathways dependent on oxidation and externalization of phosphatidylserine.

196 le of the hair cells, nor does it elicit the externalization of phosphatidylserine.

197 ace CD62L expression was not associated with externalization of phosphatidylserine.

198 ragmentation and probably occurring prior to externalization of PS as well.

199 f reactive oxygen species with oxidation and externalization of PS but not of the other major aminoph

200 Finally, externalization of PS by necroptotic cells drives recogn

201 icant decrease in lysosomal Ca2+ release and externalization of PS in response to apoptotic stimuli.

202 luorescently-tagged Annexin V to observe the externalization of PS on the plasma membrane of isolated

203 holesterol-dependent lipid assemblies in the externalization of PS, we measured the activities of two

204 ities of lipid translocators involved in the externalization of PS.

205 ly 40% via a mechanism that does not involve externalization of receptors from an internal pool.

206 The studies also show that externalization of some proteins reported to have physio

207 s of Sdc4-null mice abrogates injury-induced externalization of TG2, thereby preventing profibrotic c

208 ded by a rapid T-cell receptor (TCR)-induced externalization of the annexin-1 receptor.

209 tional changes to the capsid that enable the externalization of the capsid protein (VP) N termini, in

210 (i) both syntaxin isoforms increase the net externalization of the ENaC channel complex, (ii) that t

211 This produces autocatalytic cell death, externalization of the enzyme, and presumably cross-link

212 C. pneumoniae infection in vitro elicits the externalization of the lipid phosphatidylserine on the s

213 This expansion results in the externalization of the myristoylated capsid protein VP4

214 s prevent "breathing" motions, the transient externalization of the N-terminal regions of VP1 and VP4

215 to resolve a current controversy concerning externalization of the stromal interaction molecule STIM

216 Exposure to low pH facilitates the externalization of the viral protein 1 unique region (VP

217 are implicated in cell entry, including the externalization of the viral protein VP4 and the N termi

218 In vitro, this externalization of the VP1 amino termini is accompanied

219 rtant respects, namely, expulsion of VP4 and externalization of the VP1 N-terminal arm.

220 e first time, that acidification induces the externalization of the VP3 and possibly VP2 N termini, p

221 Externalization of these entities is followed by release

222 Externalization of this phospholipid is catalysed by scr

223 TV surgery, the use of epicardial leads and externalization of transvenous leads to the TV can avoid

224 PC6 initiates calcium influx that results in externalization of TRPC5.

225 expression did not affect carbachol-induced externalization of TRPC6 but increased Ca(2+) entry thro

226 ent-related deaths, and no patient developed externalization of tumor or metastatic disease.

227 t-related deaths and no patient demonstrated externalization of tumor or metastatic disease.

228 However, externalization of VP1 N termini appears to be unaffecte

229 The site for externalization of VP1/VP4 or release of RNA is likely b

230 VP2 N termini, presumably in prelude to the externalization of VP1u at pH 4.0, which is essential fo

231 sid protein beta barrels, accompanied by the externalization of VP4 and the N terminus of VP1.

232 ntraprotomeric loops is noteworthy since the externalization of VP4, part of VP1, and RNA during the

233 Externalizations often serve personal and social functio

234 ss in the aneurysmal segment reinforces CD36 externalization on RBCs and platelets as well as the for

235 optotic bodies (efferocytosis) is enabled by externalization on the cell target of phosphatidylserine

236 y together with increased phosphatidylserine externalization on the outer plasma membrane, a hallmark

237 Phosphatidylserine externalization on the surface of dying cells is a key s

238 CD45 is not required for phosphatidylserine externalization or DNA degradation during galectin-1 dea

239 sely, IL-31 had no effect on CD63 and CD203c externalization or histamine release.

240 PAPANONOate, however, had no effect on PS externalization or other markers of apoptosis following

241 g the existence of a significant restorative externalization pathway.

242 n, DNA fragmentation, and phosphatidylserine externalization prior to cell death.

243 L-1beta from LPS/ATP-treated BMDMs, but this externalization process is not selective for cytokines a

244 ovide the first structural evidence that the externalization process occurs at the protein interface

245 pectedly, our studies revealed that cellular externalization, rather than transcription of Pfn1, is a

246 Selective oxidation of PS precedes its externalization/recognition and is essential for the PS-

247 ation, we hypothesized that it may affect PS externalization/recognition without affecting other feat

248 Although LLSP externalization remains poorly understood, some possible

249 n freshly dissected mouse retina detected PS externalization restricted to POS tips with discrete bou

250 ule on Jurkat cytoplasts induces dramatic PS externalization similar to that observed during apoptosi

251 induced PARP cleavage and phosphatidylserine externalization, suggesting that ERK activity coincided

252 n Tmc1 cause constitutive phosphatidylserine externalization that correlates with deafness phenotype.

253 Scramblase enzymes carry out cellular PS externalization; thus, we targeted these proteins in ord

254 he GPIbalpha and beta1 integrin, and reduced externalization to megakaryocyte and platelet membranes.

255 via autocrine/paracrine functions following externalization to the outer side of the plasma membrane

256 hatidylserine followed by phosphatidylserine externalization upon exposure to cumene hydroperoxide.

257 o invasive biopsy to avoid the risk of tumor externalization, vision impairment, and other side effec

258 PS externalization was accompanied by inhibition of aminoph

259 rombosis, we observed, unexpectedly, that PS externalization was concentrated at the vessel wall, not

260 oPC-induced TRPC6-CaM dissociation and TRPC6 externalization was disrupted.

261 ondensation/fragmentation suggesting that PS externalization was dissociated from the common apoptoti

262 Cable externalization was found to be more common in the 8-Fre

263 Infection-induced phosphatidylserine externalization was immediate, transient, calcium depend

264 Rapid prelytic phosphatidylserine externalization was induced in Jurkat target cells by bo

265 The extension of phosphatidylserine externalization was slowed and delayed in Wallerian dege

266 is of poly(ADP-ribose) polymerase, and 4) PS externalization were accelerated in cells overexpressing

267 CPP32 activation, fodrin proteolysis, and PS externalization were all inhibited in the presence of pe

268 cytochrome c release and phosphatidylserine externalization were attenuated by Z-VDVAD-FMK and parti

269 the ICU control group, cytosolic Ca2+ and PS externalization were comparable with healthy controls, w

270 Acidification and phosphatidylserine externalization were found to occur concurrently.

271 membrane cholesterol and phosphatidylserine externalization were increased, fostering RBC-macrophage

272 e spectral cues that give rise to a sense of externalization; when spectral cues are unnatural, sound

273 ucial link between caspase activation and PS externalization, which triggers phagocytosis of apoptoti

274 d polarity, manifested as phosphatidylserine externalization, which was significantly delayed and pro

275 Thus, CRT induced nitrosylation and its externalization with PS could explain how CRT acts as a

276 ected mutants of TG2 GTP binding (K173L) and externalization (Y274A) sites did not stimulate chondroc