ライフサイエンスコーパス: blebbing

1 nd alphaE-catenin suppressed plasma membrane blebbing.

2 latory light chain (RLC) to promote membrane blebbing.

3 tem (T3SS) of P. aeruginosa was required for blebbing.

4 aracterized by actin reorganization and cell blebbing.

5 r membrane and causes characteristic nuclear blebbing.

6 ear condensation/fragmentation, and membrane blebbing.

7 c machinery, and extensive cortical membrane blebbing.

8 croM) were nonlethal but induced significant blebbing.

9 PSK2 to induce cell contraction and membrane blebbing.

10 f a farnesyltransferase inhibitor on nuclear blebbing.

11 eoplasmic aggregates and produced no nuclear blebbing.

12 mes associated with abnormal contractions or blebbing.

13 esulted in significant reductions in nuclear blebbing.

14 ss display asymmetric furrowing and aberrant blebbing.

15 t into globular aggregates and cell membrane blebbing.

16 l death but morphologically prevent membrane blebbing.

17 ronectin and cadherin 2 function to suppress blebbing.

18 tion of Hsp27 and induced extensive membrane blebbing.

19 nts is believed to be important for membrane blebbing.

20 ytoskeletal re-arrangements such as membrane blebbing.

21 not RGS3, caused cell rounding and membrane blebbing.

22 chromatin condensation and nuclear membrane blebbing.

23 ght chain kinase (MLCK) inhibitors decreased blebbing.

24 ractions cause cell contraction and membrane blebbing.

25 ation is not needed for ROS-induced membrane blebbing.

26 toplasmic and nuclear condensation, and cell blebbing.

27 resence in the supernatant was not due to OM blebbing.

28 tion of cytoplasmic organelles, and membrane blebbing.

29 ropel themselves, including by pseudopods or blebbing.

30 rtex, which may pressurize the cytoplasm for blebbing.

31 e RhoC signaling during cell contraction and blebbing.

32 palatal shelf development, and subepidermal blebbing.

33 ensive cell contraction followed by membrane blebbing.

34 Pearling thus differs from blebbing.

35 s them susceptible to toxin-induced membrane blebbing.

36 f target cells inhibits VLY-induced membrane blebbing.

37 ne protrusions that resemble plasma membrane blebbing.

38 membrane processes such as phagocytosis and blebbing.

39 g membrane-to-cortex attachment and membrane blebbing.

40 macrophages initiated a distinct "tethered" blebbing 10 min after ATP addition.

41 a(2+)-dependent swelling (-80%) and membrane blebbing (-90%); 3) reduced calpain-dependent protein cl

42 The same treatment induced membrane blebbing, a morphological change typical of apoptosis, 1

43 sion induced excessive nonapoptotic membrane blebbing, a physiological process involved in both cytok

44 /-) megakaryocytes exhibited plasma membrane blebbing accompanied by a decreased association of the m

45 Membrane blebbing accompanies various cellular processes, includi

46 tively reproduces the monotonic decay of the blebbing activity and accounts for the lag phase in the

47 period whose duration depends on the cell's blebbing activity.

48 Also, glibenclamide prevented cell blebbing after ATP depletion, whereas blebbing was produ

49 eased viability and phenotypically different blebbing after exposure to the injury stimulus.

50 d increased the formation of plasma membrane blebbings, all these changes and activities being associ

51 Cell contraction and blebbing also frequently occur as part of the cytopathic

52 The ability of DIP to trigger blebbing also suggests a role for mDia2 in the assembly

53 ed cell death is not accompanied by membrane blebbing, although phosphatidylserine externalization an

54 on of Krtap5-5 from cancer cells led to cell blebbing and a loss of keratins 14 and 18, in addition t

55 red for entotic invasion, which is driven by blebbing and a uropod-like actin structure at the rear o

56 orylation is critical for apoptotic membrane blebbing and also implicate Rho signaling in these activ

57 oxidant injury can induce RPE cell membrane blebbing and alter RPE expression of matrix metalloprote

58 totic phenotypes, anaphase-specific cortical blebbing and asymmetric spindle pole movement.

59 ction, and MLCK inhibition led to persistent blebbing and attenuated cell volume recovery.

60 SF1-transfected 293-T cells exhibit membrane blebbing and can be rescued by the addition of a caspase

61 I or Rho-kinase (ROCK) activity inhibits NCC blebbing and causes reduced NCC EMT.

62 , increase caspase activity, cause apoptotic blebbing and cell death, and finally induce coral bleach

63 ation, and AK-B knockdown can induce nuclear blebbing and cell death.

64 13-acetate-stimulated cells, caused membrane blebbing and cell loss.

65 , we show that hyen D induces rapid membrane blebbing and cell necrosis.

66 rin-ligand interaction induces both membrane blebbing and changes in membrane permeability.

67 mains additionally induced cell rounding and blebbing and conferred enhanced sensitivity to osmotic s

68 nlethal injury with HQ upregulated nonlethal blebbing and decreased ECM turnover.

69 Inhibition of NHE1 disrupts membrane blebbing and decreases changes in membrane permeability.

70 eral increase in lipid order associated with blebbing and dissolution of the cells.

71 sembled vesicles and, in some cases, promote blebbing and division.

72 e lacking gelsolin had delayed onset of both blebbing and DNA fragmentation, following apoptosis indu

73 um response factor) pathway for sustained PM blebbing and entotic invasion.

74 al DNA cleavage, plasma membrane and nuclear blebbing and formation of apoptotic bodies, are not obse

75 sonized Daudi B cells induces rapid membrane blebbing and generation of long, thin structures protrud

76 Our observations that blebbing and IL-1 beta release are dissociable suggest t

77 e actin cortex in cells during initiation of blebbing and in blebs at different stages of their expan

78 ells to nonlethal oxidant injury upregulated blebbing and increased pro-MMP2 protein, but downregulat

79 nhibition of Rac1 activity restored membrane blebbing and increased ROCK activity in Rap1GAP-depleted

80 ility, and establish a link between membrane blebbing and integrin signaling.

81 These markers included membrane blebbing and internucleosomal DNA fragmentation.

82 rane organization, including plasma membrane blebbing and invagination, vacuolation and fragmentation

83 ally and structurally distinct from membrane blebbing and involves disruption to the platelet microtu

84 the evagination occurs via a process akin to blebbing and is not driven by actin polymerization.

85 rop in cell height potentiated by persistent blebbing and loss of cortical F-actin homogeneity.

86 rigidity, which resulted in a dose-dependent blebbing and lysis of erythrocytes.

87 ADAM17, as well as membrane events, such as blebbing and microparticle production.

88 support the hypothesis that HQ may regulate blebbing and molecules that influence ECM turnover.

89 tion state is a major determinant of nuclear blebbing and morphology via its contribution to nuclear

90 MTX also induces membrane blebbing and nonselective pores similar to those elicite

91 nuclear deformation that may lead to nuclear blebbing and nuclear envelope rupture.

92 pical apoptotic features such as cytoplasmic blebbing and nuclear fragmentation were seen within 6 hr

93 novel function for NHE1 and NCX1 in membrane blebbing and permeability, and establish a link between

94 cells in safeguarding neurons against axonal blebbing and poliomyelitis from murine betacoronavirus-i

95 eorganization, cytoplasm shrinkage, membrane blebbing and protein-tyrosine phosphorylation.

96 protruding membranes explains the excessive blebbing and protrusion observed in septin-deficient T c

97 n of markers of apoptosis including membrane blebbing and stimulation of caspase-3-like activity.

98 m rapidly destabilizes proplatelets, causing blebbing and swelling.

99 ion can cause apoptosis-independent cellular blebbing and that this process is mediated by the Rho/Rh

100 Both the dynamics of blebbing and the connection to nuclear pore biogenesis r

101 echanism of proliferation involving membrane blebbing and tubulation, which is dependent on an altere

102 ision machinery and in occurring by membrane blebbing and tubulation.

103 c cells, which are disintegrated by membrane blebbing and vesiculation, aging lens fiber cells are co

104 permeable channel; it also leads to membrane blebbing and, in certain immune cells, interleukin-1beta

105 eep cells to have protracted plasma membrane blebbing, and a defect in plasma membrane recruitment of

106 nges that include cell contraction, membrane blebbing, and apoptotic body formation.

107 gonucleosomal ladder formation, cell surface blebbing, and apoptotic body formation.

108 gonucleosomal ladder formation, cell surface blebbing, and apoptotic body formation.

109 ation, nanopore-conducted currents, membrane blebbing, and cell death.

110 , the loss of focal adhesion sites, membrane blebbing, and cell detachment.

111 hanced caspase 9 activation, plasma membrane blebbing, and drug-induced cytotoxicity.

112 ng, clathrin-mediated endocytosis, polarized blebbing, and endocytic vesicle sorting.

113 tin condensation and fragmentation, membrane blebbing, and formation of apoptotic bodies.

114 ns, including asymmetric furrowing, membrane blebbing, and impaired cytokinesis.

115 separation and endothelial cell detachment, blebbing, and necrosis have been observed after ischemia

116 properties such as pore dilatation, membrane blebbing, and phosphatidylserine exposure that were prev

117 spreading, characterized by profuse membrane blebbing, and prevents the formation of membrane ruffles

118 e in cellular Tropomyosin-3, plasma membrane blebbing, and release of 0.1- to 1-mum-diameter MPs.

119 is accompanied by nuclear volume expansion, blebbing, and rupture, ultimately resulting in reduced c

120 ing under agarose, which efficiently induces blebbing, and the dynamics of membrane deformations were

121 avage into 180 bp fragments, plasma membrane blebbing, and the formation of apoptotic bodies do not o

122 lanoma cells from actin-driven protrusion to blebbing, and we present tools to quantify how cells man

123 e were used to study injury-induced membrane blebbing, and XTT conversion was used to detect cell via

124 any of the EMPs in HEK-293 cells led to cell blebbing, annexin V binding, and cell death, by a caspas

125 al cytological changes that include membrane blebbing, appearance of ghost nuclei, cell swelling, and

126 Using nuclear envelope (NE) blebbing as a phenotypic measure, we establish a direct

127 plicates amoeboid-type motility and membrane blebbing as features that may facilitate invasion throug

128 lar membranes, membrane disorganization, and blebbing as well as cytoplasmic vacuolization.

129 crease in heterochromatin suppresses nuclear blebbing associated with nuclear rupture and DNA damage.

130 loss of OM material through vesiculation and blebbing at cell-division sites and compensatory shrinka

131 Moreover, Ca(2+) can induce some blebbing at mM concentrations but not nearly as effectiv

132 trikingly, cells lacking DipM also showed OM blebbing at the division site, at cell poles and along t

133 dition for processes such as pore formation, blebbing, budding, and vesicularization, all of which de

134 henotype; MAP2c not only caused cessation of blebbing but also induced the formation of two distinct

135 xidant injury causes increased cell membrane blebbing but decreased activation of MMP-2.

136 atment induced early rounding and occasional blebbing but not late apoptotic events, blistering, and

137 etion are associated with glial swelling and blebbing, but mechanisms involved in these effects remai

138 ells, which were elongated and had extensive blebbing, but no lamellipodia or ruffle formation.

139 ater times, this rac mutant induces membrane blebbing, but not apoptosis.

140 easurements suggest that Zn(2+) caused lipid blebbing by decreasing the area per lipid on the side of

141 as also needed for the induction of membrane blebbing by PSK2, which was itself a substrate for caspa

142 Blebbing can be divided into three distinct phases: bleb

143 Act evoked cell membrane blebbing, caspase 3-cleavage, and activation of caspases

144 is, including nuclear condensation, membrane blebbing, caspase activation, and DNA laddering.

145 eflected by chromatin condensation, membrane blebbing, cell detachment, and loss of mitochondrial mem

146 poptosis, which is characterized by membrane blebbing, cell rounding, and subsequent loss of cell-mat

147 logic signs of apoptosis, including membrane blebbing, cell shrinkage, and apoptotic body formation.

148 indicative of apoptosis, including membrane blebbing, cell shrinkage, condensation of nuclear chroma

149 chain (MLC) phosphorylation was increased in blebbing cells and that MLC phosphorylation was prevente

150 Blebbing cells are strongly chemotactic to cyclic-AMP, p

151 Recent experiments involving blebbing cells have led to conflicting hypotheses regard

152 kinase inhibitors performed on synchronized blebbing cells indicated that only myosin light chain ki

153 When we locally perfuse blebbing cells with cortex-relaxing drugs to dissipate p

154 counts for the lag phase in the spreading of blebbing cells.

155 However, inhibition of NCX1 enhances cell blebbing; cells become swollen because of NHE1 induced i

156 ibited a novel color segregation phenotype, "blebbing," characterized by minisatellite instability du

157 e independent approaches, including membrane blebbing, chromosome condensation and fragmentation, DNA

158 on of host and AcMNPV DNA, and cell membrane blebbing coincided with the initiation of viral DNA synt

159 to biphasic propidium dye uptake and dilated blebbing coincident with cytolysis.

160 pecifically cell shrinkage, dynamic membrane blebbing, condensation of chromatin, and DNA fragmentati

161 hanced annexin-V binding, extensive membrane blebbing, condensation of heterochromatin, and cell frag

162 ing drugs to dissipate pressure on one side, blebbing continues on the untreated side, implying non-e

163 This inhibition of cellular blebbing correlated with a 25% decrease in cytosolic fre

164 ath characterized by cell rounding, membrane blebbing, cytochrome c release, procaspase-3 and poly(AD

165 were induced by 5H7, including cell membrane blebbing, cytoplasmic vacuolization, condensation of nuc

166 s exhibited increased membrane permeability, blebbing, cytoplasmic vacuolization, swollen mitochondri

167 ebbing (which slow detachment does not), and blebbing decreases with time in a dynamin-dependent fash

168 videnced by the induction of plasma membrane blebbing, DNA fragmentation, and cleavage of the caspase

169 phenol, however, did exhibit plasma membrane blebbing, DNA fragmentation, and phosphatidylserine relo

170 h, we have found that NK1R-mediated cellular blebbing does not associate with apoptosis.

171 Membrane blebbing during the apoptotic execution phase results fr

172 statin is a small molecule that affects cell blebbing during the process of cell division, which has

173 and functional effects on invasion, membrane blebbing dynamics, and osmotic water permeability were a

174 activation signals distinct, novel membrane blebbing events (dependent on RhoA activation and Rho-ef

175 of the outer membrane and to severe membrane blebbing eventually progressing to lysis.

176 tokinesis, actin-dependent motility and cell blebbing, eventually abrogating gastrulation.

177 ted from RBL-2H3 cells by chemically induced blebbing exhibit a degree of phospholipid saturation tha

178 hagocytic but not channel, pore, or membrane-blebbing function, and double-transfected P2X7L and P2X7

179 Such findings have implications for blebbing, fusion, oxidation, and related properties of P

180 oid features such as cell rounding, membrane blebbing, high levels of contractility, and increased in

181 hrombin receptor PAR4 triggers cell membrane blebbing in a RhoA-and beta-arrestin-dependent manner.

182 20-kDa light chain of myosin II (MLC20) with blebbing in apoptotic cells.

183 mbly coupled with a low frequency of nuclear blebbing in arrested oocytes negatively impacts embryoni

184 A/myosin-II contractility to further augment blebbing in confinement.

185 nd may contribute to injury-induced membrane blebbing in differentiated RPE cells.

186 We induced membrane blebbing in human HT1080 fibrosarcoma cells by inhibitin

187 r rigidity, which results in reduced nuclear blebbing in lamin B1 null nuclei.

188 ermeability and FGF-induced dynamic membrane blebbing in LEC and thereby drives invasion and patholog

189 growth factor (FGF)-induced dynamic membrane blebbing in LEC, which is sufficient to augment invasion

190 coordinated with dramatic, nuclear membrane blebbing in oocytes.

191 ts, induces actin rearrangement and membrane blebbing in RPE cells as well as sub-RPE deposits in mic

192 owing after nocodazole release and excessive blebbing in the presence of nocodazole).

193 ns, and VLY-induced epithelial cell membrane blebbing in the vaginal mucosa may play a role in the pa

194 The transition to blebbing in these conditions occurred through an interme

195 as well as nonapoptotic plasma membrane (PM) blebbing in this cellular motile process.

196 the proportion of cells with plasma membrane blebbing in TLVM and with increased side scattering prop

197 Cyclic-AMP induces transient blebbing independently of much of the known chemotactic

198 Similarly, target membrane blebbing induced by CTL via the FasL/Fas, but not via th

199 of septins was also evident during excessive blebbing initiated by blocking membrane trafficking with

200 llular calcium increase, indicating that the blebbing is a process independent of intracellular calci

201 Blebbing is a protein kinase C-independent process, sinc

202 Since nonapoptotic membrane blebbing is now recognized as an important regulator of

203 created when optical density caused by cell blebbing is plotted as a function of time.

204 tions support a model where nuclear membrane blebbing is required to increase the trafficking of nucl

205 We find that cortical blebbing is tightly coupled to MRTF nuclear shuttling to

206 ship between integrin signaling and membrane blebbing is unclear.

207 theoretical concepts, seeking information on blebbing itself, and on cytomechanics in general.

208 iation of the apoptotic process are membrane blebbing, loss of focal adhesion sites, and retraction f

209 ncentration in turn triggers plasma membrane blebbing, lysosomal exocytosis, and membrane repair resp

210 nvert border cells to a round morphology and blebbing migration mode.

211 ated sarcoplasmic vesicles, nuclear membrane blebbing, mitochondrial swelling, nuclear inclusions, an

212 Integrin signaling and membrane blebbing modulate cell adhesion, spreading, and migratio

213 onse to CA-4-P, some cells rapidly assumed a blebbing morphology in which F-actin accumulated around

214 s the only missense mutation reported in any blebbing mutant or individual with Fraser syndrome, sugg

215 heir extensive phenotypic overlap, the mouse blebbing mutants have been considered models of this dis

216 es a rapid retraction of processes, membrane blebbing, nuclear collapse, and cell death.

217 totic features like cell shrinkage, membrane blebbing, nuclear condensation and DNA fragmentation.

218 ition, sAC inhibition reversed BSIA membrane blebbing, nuclear condensation, and DNA fragmentation.

219 s display apoptotic signs including membrane blebbing, nuclear condensation, and reduction of mitocho

220 hypoxia, as revealed by sarcolemmal membrane blebbing, nuclear fragmentation, and chromatin condensat

221 ed cells displayed apoptosis-associated cell blebbing, nuclear pyknosis and fragmentation (karyorrhex

222 s, we establish that PAR4-dependent membrane blebbing occurs independently of the Galpha (q/11)- and

223 atform, we demonstrate that nuclear envelope blebbing occurs rapidly and synchronously immediately af

224 The model provides conditions under which blebbing occurs, and naturally gives rise to traveling b

225 structuring, characterized by effacement and blebbing of its apical surface.

226 n was accompanied by and appeared to precede blebbing of the cell membrane, suggesting participation

227 pressed E-cadherin in RK3E cells and induced blebbing of the cytoplasmic membrane.

228 as chromatin condensation in the nucleus and blebbing of the membranes.

229 misplacement and abnormal beating of cilia, blebbing of the microvilli.

230 Blebbing of the outer membrane and increase in membrane

231 at these points of distortion by removal or blebbing of the outer membrane leaflet.

232 sis (vigorous "boiling" of the cytoplasm and blebbing of the plasma membrane) for 10-20 min, with sub

233 mic reticulum and outer nuclear envelope and blebbing of the plasma membrane, as seen by transmission

234 WCR, injury to the midgut was manifested by "blebbing" of the midgut epithelium into the gut lumen.

235 involving hypertonic stress causes membrane 'blebbing' of the Xenopus oocyte and the shedding of plas

236 is sufficient to increase nuclear volume and blebbing on two-dimensional surfaces, and acts synergist

237 dation, but were not separable from membrane blebbing or cell lysis in this cell line.

238 ganglion cells, but did not lead to membrane blebbing or increased permeability to Yo-Pro-1.

239 esulted in a striking improvement in nuclear blebbing (P < 0.0001 by chi2 statistic).

240 The Deltazrt1 blebbing phenotype is partially dependent on a functiona

241 rom mutant Krt75 mouse models reproduced the blebbing phenotype when grafted in vivo.

242 of the P2X(7) receptor and might mediate the blebbing phenotype, identified epithelial membrane prote

243 e nuclear envelope would improve the nuclear blebbing phenotype.

244 P2X(7) receptor is responsible for the cell blebbing phenotype.

245 oinjection of tau or mature MAP2 rescued the blebbing phenotype; MAP2c not only caused cessation of b

246 ransmembrane potential dissipation, membrane blebbing, phosphatidylserine exposure, DNA damage and ch

247 ent facilitation, membrane permeabilization, blebbing, phospholipid scrambling, inflammasome activati

248 In this article, we demonstrate that cell blebbing plays a critical role in the global mechanical

249 find that loss of cell adhesion and membrane blebbing precede filopodial extension and the onset of m

250 ent of MLC phosphorylation in regulating the blebbing process.

251 Unlike blebbing, procoagulant ballooning is irreversible and a

252 leb expansion while also predicting that the blebbing rate is impaired by elevating the concentration

253 Genetically, blebbing requires myosin-II and increases when actin pol

254 After removal of transient oxidant exposure, blebbing resolved and RPE MMP-2 activity and protein rec

255 egradation and significant increases in cell blebbing, rounding-up, and overall size.

256 t with the loss of processes and cytoplasmic blebbing seen in cells undergoing apoptosis.

257 lding and causing the characteristic nuclear blebbing seen in HGPS cells.

258 in had distinct apoptotic features (membrane blebbing, shrinkage, cellular fragmentation), but those

259 nd 2 (ERK-1/2) were shown to protect against blebbing since blebbing was attenuated on ERK-1/2 stimul

260 Minisatellite tract alterations in blebbing strains consist exclusively of the loss of one

261 A physical model of blebbing suggests that detachment of the cell membrane i

262 C3 transferase inhibited apoptotic membrane blebbing, supporting a role for a Rho family member in t

263 vesicles produced from nonspecific membrane "blebbing." Taken together, our results demonstrated that

264 rug-induced plasma membrane permeability and blebbing, terminal deoxynucleotidyl transferase dUTP nic

265 apoptosis within 48-72 h, marked by nuclear blebbing, terminal deoxynucleotidyl transferase-mediated

266 studies show that patch formation occurs via blebbing that disrupts normal membrane structure and red

267 During blebbing, the membrane detaches from the cortex and infl

268 ppreciation of physiological significance of blebbing, the molecular and, especially, structural mech

269 ll-cell adhesion and suppression of membrane blebbing, thereby enabling proper radial intercalation.

270 cancerous single-cells transitioning from a blebbing to a pseudopodial morphology.

271 Furthermore, PM blebbing triggered SRF-mediated up-regulation of the met

272 cytoplasmic; swelling, dendritic retraction, blebbing, vacuolization, which are all characteristics o

273 poptosis, including cell shrinkage, membrane blebbing, vesicle release, and chromatin condensation an

274 P2X7R-dependent blebbing was abrogated in the presence of Rho-effector k

275 Blebbing was also completely inhibited by ML-9, a myosin

276 Finally, blebbing was also inhibited by disruption of the actin c

277 Dose-dependent blebbing was also observed during microscopic analysis.

278 Blebbing was associated with decreased cell viability an

279 were shown to protect against blebbing since blebbing was attenuated on ERK-1/2 stimulation and was u

280 This blebbing was comparably induced by the P2X7R-selective a

281 DIP-induced blebbing was dependent on mDia2 but did not require the

282 for biased signaling in PAR4 since membrane blebbing was dependent on some, but not all, signaling p

283 Cell membrane blebbing was detected using GFP-membrane-labeled RPE cel

284 Blebbing was initiated at ATP concentrations > or = 3 mM

285 However, rapid induction of membrane blebbing was not inhibited by z-DEVD-CH2F.

286 d cell blebbing after ATP depletion, whereas blebbing was produced by exposure to diazoxide.

287 CA-4-P-mediated contractility and blebbing were associated with a Rho-dependent increase i

288 ape transformations that is complementary to blebbing, where the plasma membrane detaches from the ac

289 Abrupt cell detachment leads to pronounced blebbing (which slow detachment does not), and blebbing

290 odazole, BMI-1026 induced excessive membrane blebbing, which appeared to be caused by formation of ec

291 es of human cells and caused plasma membrane blebbing, which compromised membrane integrity and proba

292 e each measurement before the cell undergoes blebbing, which is associated with a considerable increa

293 We propose that membrane blebbing, which is known to occur under specific physiol

294 y doses caused a moderate amount of membrane blebbing, which was well tolerated by differentiated ARP

295 expression also affected nsPEF-induced cell blebbing, with only 20% of the silenced cells developing

296 Whereas HEK-P2X7 cells exhibit zeiotic blebbing within 5 min of ATP treatment, BAC1 macrophages

297 atly delayed in maturation, (ii) substantial blebbing within chlamydial inclusions, and (iii) electro

298 atin results in a softer nucleus and nuclear blebbing, without perturbing lamins.

299 , an actin polymerizing agent known to cause blebbing, yielded results similar to the depolymerizing

300 organelle condensation, cytoplasmic membrane blebbing (zeiosis), and chromatin condensation and margi