ライフサイエンスコーパス: externalization

1 ible to the dye or antibodies, demonstrating externalization.

2 /oxidation and inhibition of APLT causing PS externalization.

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

4 , caspase activation, and phosphatidylserine externalization.

5 l membrane potential, and phosphatidylserine externalization.

6 Sickle RBCs exhibit a wide range of PS externalization.

7 hrough the modulation of membrane PS residue externalization.

8 caspase-3 activation and phosphatidylserine externalization.

9 y, DNA fragmentation, and phosphatidylserine externalization.

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

11 apoptosis, including phosphatidylserine (PS) externalization.

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

13 at different pHout and mechanisms of urease externalization.

14 tached to the extracellular matrix following externalization.

15 crambling leading to phosphatidylserine (PS) externalization.

16 lack of CD74 and failed in subsequent CXCR7 externalization.

17 wer nsPEF exposure parameters compared to PS externalization.

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

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

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

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

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

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

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

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

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

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

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

29 toposide as determined by phosphatidylserine externalization and caspase activation.

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

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

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

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

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

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

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

37 2O2)-induced apoptosis was accompanied by PS externalization and oxidation of different phospholipids

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

63 (100 microm), as shown by phosphatidylserine externalization, caspase-3 activation, development of a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 Phosphatidylserine externalization is associated with cellular development,

101 PS externalization is generally attributed to an increase i

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

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

104 This externalization most likely is effected by cell death an

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

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

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

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

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

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

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

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

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

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

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

116 pecific insulation abrasion characterized by externalization of conductor cables.

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

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

119 Externalization of IL-1 beta required active recognition

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

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

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

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

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

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

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

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

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

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

130 Externalization of phosphatidylserine after Ca/P stimula

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

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

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

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

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

136 The rapid externalization of phosphatidylserine by infected cells

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

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

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

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

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

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

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

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

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

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

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

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

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

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

151 through pathways dependent on oxidation and externalization of phosphatidylserine.

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

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

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

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

156 Finally, externalization of PS by necroptotic cells drives recogn

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 Externalization of these entities is followed by release

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

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

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

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

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

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

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

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

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

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

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

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

187 g the existence of a significant restorative externalization pathway.

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

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

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

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

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

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

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

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

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

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

198 PS externalization was accompanied by inhibition of aminoph

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

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

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

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

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

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

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

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

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

208 Acidification and phosphatidylserine externalization were found to occur concurrently.

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

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

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

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

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

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