ライフサイエンスコーパス: CME

1 CME initiates by recruitment of adaptors and clathrin to

2 CME is initiated by the formation of clathrin-coated pit

3 CME is shut down during early mitosis, but the mechanism

4 CME suppression was also phenocopied by HSC70 RNAi deple

5 in I and II in vitro and in cells (IC((5)(0)(CME)) = 1.9 muM).

6 oidal organization (P<0.001), VMT (P<0.001), CME (P<0.001), exudation (P<0.001), and disruption of th

7 iew." Subscribers can receive 1.5 category 1 CME credits by completing the CME quiz that accompanies

8 CME and intraretinal fluid (IRF) status: (1) CME, (2) IRF without CME, (3) neither CME nor IRF.

9 y block (n = 1), choroidal effusion (n = 2), CME (n = 4), and redislocation (n = 1) in the exchange g

10 ex (TPC), which is proposed to function as a CME adaptor complex, is only conserved in plants and a f

11 cells by inhibition of GSK3beta accelerates CME, alters CCP dynamics and, unexpectedly, increases th

12 Readers can complete the accompanying CME quiz for 1.5 credits.

13 CLCb/Dyn1-dependent adaptive CME selectively altered EGF receptor trafficking, enhanc

14 We define molecular mechanisms for adaptive CME in cancer cells and a role for the reciprocal crosst

15 This "adaptive CME" resulted from upregulation of dynamin-1 (Dyn1) and

16 cells contributes to a program of "adaptive" CME that alters signaling to enhance cancer cell surviva

17 vitreal aflibercept injection for addressing CME in RP seems to be an effective treatment.

18 The extended longitudinal resection after CME with CVL increased the nodal yield but did not incre

19 r confounding factors) for vitreous cell and CME for those treated with cryotherapy compared to contr

20 of anterior chamber cell, vitreous cell, and CME in the cryotherapy-treated eyes.

21 ng the more potent inhibitors of dynamin and CME yet reported.

22 Hard exudates and CME regressed completely in 15 of 15 and 5 of 6 eyes, re

23 inoma (SCLC) primary xenograft model, ME and CME compounds were found to be highly potent in inhibiti

24 (IC50 = 10.6 +/- 1.3 to 1.6 +/- 0.3 muM) and CME (IC50(CME) = 65.9 +/- 7.7 to 3.7 +/- 1.1 mM), which

25 use of aflibercept in a patient with RP and CME.

26 e reciprocal crosstalk between signaling and CME in cancer progression.

27 ind that the positively curved membranes are CME hotspots, and that key CME proteins, clathrin and dy

28 hort CCS intensity trace fragments to assess CME dynamics.

29 required for efficient Ede1 localization at CME sites are the third EH domain, the proline-rich regi

30 groups were created on the basis of baseline CME and intraretinal fluid (IRF) status: (1) CME, (2) IR

31 Because CME entails substantial local remodeling of the plasma m

32 we found no significant association between CME prevalence and UIC based on the entire sample as tes

33 phostinA23, which is routinely used to block CME, displays similar properties, thus questioning its u

34 sures were changes in anterior segment cell, CME, visual acuity, and IOP and development of a visuall

35 In nonneuronal cells, CME of the majority of transmembrane receptors is either

36 s near Earth and Mars confirm the channelled CME motion, and are consistent with an ellipse shape of

37 Chronic CME was the most common cause of MVL (3.55%), and macula

38 Classical CME proceeds via the formation of clathrin-coated pits (

39 namin recruitment, consistent with classical CME.

40 Ca(2+)- and stimulus-dependent compensating CME in mature IHCs.

41 Analysis of constitutive CME is difficult because the initiation of endocytic eve

42 critical specifically for activity-dependent CME of synaptic glutamate receptors.

43 -attached capacitance measurements to detect CME of single vesicles in a millisecond time resolution

44 images of sufficient quality for determining CME and IRF at baseline, 92 (8.1%) had CME, 766 (67.7%)

45 in the follow-up cohort, 105 (40%) developed CME during a median follow-up of 31 months (mean, 34; ra

46 eroid therapy none of the patients developed CME subsequently (P = .003).

47 significantly reduced the odds of developing CME as compared to topical corticosteroids in nondiabeti

48 significantly reduced the odds of developing CME as compared to topical corticosteroids in nondiabeti

49 rticosteroids reduced the odds of developing CME in nondiabetic and diabetic patients, as compared to

50 significantly reduced the odds of developing CME, as compared to topical corticosteroids, in nondiabe

51 During CME in yeast, actin polymerization is triggered and coor

52 During CME, endocytic adaptor proteins bind cargoes at the cell

53 dynamics and premature actin assembly during CME through a PtdIns(4,5)P2-dependent mechanism.

54 temporal regulation of actin assembly during CME.

55 lymerization promotes vesicle fission during CME by inducing cholesterol-dependent membrane reorganiz

56 erization may promote vesicle fission during CME by providing direct mechanical forces.

57 rol might function in vesicle fission during CME in the same pathway.

58 that the dynamics of vesicle fission during CME is Ca(2)(+) dependent but becomes Ca(2)(+) independe

59 tin polymerization in vesicle fission during CME.

60 itment and actin polymerization onset during CME.

61 ent and function of specific proteins during CME is achieved remains unclear.

62 mportance of this "checkpoint." Dysregulated CME also alters EGF receptor signaling and leads to cons

63 mutant cells displaying rapid, dysregulated CME are defective in early endosomal trafficking, matura

64 euronal cells to trigger rapid, dysregulated CME.

65 l effusion (9.3%) and cystoid macular edema (CME) (7.0%).

66 red and evaluated for cystoid macular edema (CME) and persistence of inner retinal layers.

67 atients with resolved cystoid macular edema (CME) at month 3, those with persistent CME did worse, on

68 ecreasing the risk of cystoid macular edema (CME) in high-risk eyes, but must be used with caution in

69 urrent treatments for cystoid macular edema (CME) in retinitis pigmentosa (RP) are not always effecti

70 Cystoid macular edema (CME) in retinitis pigmentosa (RP) has been managed in se

71 Cystoid macular edema (CME) occurred in 5 eyes (0.87%): 3 in group A and 2 in g

72 e score of >/=1.5+ or cystoid macular edema (CME) of >300 mum were enrolled.

73 r pressure (IOP), and cystoid macular edema (CME) were recorded at each visit.

74 ations, resolution of cystoid macular edema (CME), and anterior chamber and vitreous inflammation wer

75 inal detachment (RD), cystoid macular edema (CME), and epiretinal membrane (ERM).

76 d by inflammation and cystoid macular edema (CME), and in uveitic patients, intensive perioperative s

77 differentiate it from cystoid macular edema (CME), and review the role of carbonic anhydrase inhibito

78 foveal architecture, cystoid macular edema (CME), intraretinal exudates and subretinal lipid aggrega

79 , retinal detachment, cystoid macular edema (CME), macular scarring, macular hole, optic neuropathy,

80 selected visits where cystoid macular edema (CME), subretinal fluid (SRF), or pigment epithelial deta

81 in eyes with uveitic cystoid macular edema (CME).

82 P) increase (n = 12), cystoid macular edema (CME; n = 3), and nonarteritic anterior ischemic optic ne

83 New models of continuing medical education (CME) seek not only to impart knowledge but to change phy

84 Loss of efficient CME in twd40-2-3 resulted in the unregulated overaccumul

85 rocesses like clathrin-mediated endocytosis (CME) across a diverse range of organisms and mechanical

86 e presence of clathrin-mediated endocytosis (CME) and bulk endocytosis.

87 urred through clathrin-mediated endocytosis (CME) and independently of choline binding protein A (Cbp

88 or uptake via clathrin-mediated endocytosis (CME) and subsequent intracellular sorting for degradatio

89 y impact cell clathrin-mediated endocytosis (CME) capacity.

90 Clathrin-mediated endocytosis (CME) constitutes the major pathway for uptake of signali

91 tion phase of clathrin-mediated endocytosis (CME) determines where and when endocytosis occurs.

92 erstanding of clathrin-mediated endocytosis (CME) dynamics is based on detection and tracking of fluo

93 s involved in clathrin-mediated endocytosis (CME) exhibits distinctive topological properties.

94 inhibitor of clathrin-mediated endocytosis (CME) in different systems and that ES9 induces inhibitio

95 e-1) inhibits clathrin-mediated endocytosis (CME) in mammalian cells by aggregate-driven sequestratio

96 and Arp2/3 in Clathrin-Mediated Endocytosis (CME) in multicellular organisms.

97 e of actin in clathrin-mediated endocytosis (CME) in yeast versus mammalian cells.

98 Clathrin-mediated endocytosis (CME) involves nanoscale bending and inward budding of th

99 Clathrin-mediated endocytosis (CME) involves the recruitment of numerous proteins to si

100 Clathrin-mediated endocytosis (CME) is a fundamental process in cell biology and has be

101 Clathrin-mediated endocytosis (CME) is a fundamental property of eukaryotic cells.

102 membrane via clathrin-mediated endocytosis (CME) is a key mechanism for regulating synaptic strength

103 Clathrin-mediated endocytosis (CME) is a key pathway for transporting cargo into cells

104 Clathrin-mediated endocytosis (CME) is a major internalization route for PM proteins.

105 eurons, where clathrin-mediated endocytosis (CME) is dramatically impaired, to gain insight into the

106 Clathrin-mediated endocytosis (CME) is facilitated by a precisely regulated burst of ac

107 we find that clathrin-mediated endocytosis (CME) is harnessed by enteroviruses to traffic cholestero

108 Clathrin-mediated endocytosis (CME) is the best-characterized type of endocytosis in eu

109 in the brain, clathrin-mediated endocytosis (CME) is the dominant mode of synaptic vesicle retrieval

110 Clathrin-mediated endocytosis (CME) is the major internalisation route for many differe

111 Clathrin-mediated endocytosis (CME) is the major mechanism for internalization in mamma

112 Clathrin-mediated endocytosis (CME) is the major route of receptor internalization at t

113 Clathrin-mediated endocytosis (CME) is used to internalize a diverse range of cargo pro

114 Clathrin-mediated endocytosis (CME) is vital for the internalization of most cell-surfa

115 Clathrin-mediated endocytosis (CME) manages the sorting and uptake of the bulk of membr

116 d and Mena in clathrin-mediated endocytosis (CME) of the EGFR.

117 ed either via clathrin-mediated endocytosis (CME) or independently of clathrin (CIE) remains segregat

118 omplex of the clathrin-mediated endocytosis (CME) pathway.

119 Clathrin-mediated endocytosis (CME) regulates many aspects of plant development, includ

120 Clathrin-mediated endocytosis (CME) regulates signaling from the plasma membrane.

121 ot abolished; clathrin-mediated endocytosis (CME) was severely impaired at the step of membrane fissi

122 ission during clathrin-mediated endocytosis (CME), and it has been proposed that actin polymerization

123 During clathrin-mediated endocytosis (CME), endocytic-site maturation can be divided into two

124 hich inhibits clathrin-mediated endocytosis (CME), impaired the AtPep1-PEPR1 internalization and comp

125 important for clathrin-mediated endocytosis (CME), the mechanistic role of Ca(2)(+) in CME remains to

126 ission during clathrin-mediated endocytosis (CME).

127 es, including clathrin-mediated endocytosis (CME).

128 hich to study clathrin-mediated endocytosis (CME).

129 ing classical clathrin-mediated endocytosis (CME).

130 resilience of clathrin-mediated endocytosis (CME).

131 important for clathrin-mediated endocytosis (CME).

132 rtant role in clathrin-mediated endocytosis (CME).

133 required for clathrin-mediated endocytosis (CME).

134 regulated by clathrin-mediated endocytosis (CME).

135 The Chemical Master Equation (CME) is a cornerstone of stochastic analysis and simulat

136 A treatment does not directly modulate ErbB2 CME rate but it affects ErbB2 recycling fate, routing th

137 on and European complete mesocolic excision (CME) with central vascular ligation (CVL) are both based

138 rom seven different space missions of a fast CME, which originated in an active region near the disk

139 Deletion of EDE1 results in fewer CME initiations and defects in the timing of vesicle mat

140 es of all CATT study eyes were evaluated for CME.

141 the CSA group were maximum lesion height for CME (r(2) value = 0.96) and B-scan count for SRF and PED

142 tinal dystrophies can be differentiated from CME by a combination of clinical examination, IVFA, and

143 These must be distinguished from CME.

144 of NSAID therapy to prevent vision loss from CME at 3 months or more after cataract surgery.

145 are at significantly higher risk for future CME.

146 y) had a significantly higher rate of future CME (n = 66; 50%) compared with eyes without subclinical

147 edge and is a well-accepted method of global CME delivery.

148 ining CME and IRF at baseline, 92 (8.1%) had CME, 766 (67.7%) had IRF without CME, and 273 (24.1%) ha

149 Of the 199 patients, 36.2% had CME in 1 or both eyes.

150 (n=22), the mean score for children who had CME (n=31) was 7.3 points (95% confidence interval [CI],

151 Compared with children who did not have CME as infants (n=22), the mean score for children who h

152 icle provides some practical ideas about how CME providers and QI experts may beneficially integrate

153 l CME is seen in premature infants; however, CME does not appear to be correlated with ROP stage.

154 .6 +/- 1.3 to 1.6 +/- 0.3 muM) and CME (IC50(CME) = 65.9 +/- 7.7 to 3.7 +/- 1.1 mM), which makes this

155 In CME and growth inhibition cell-based assays, the data ob

156 In CME, plasma membrane-binding clathrin adaptors recruit a

157 omplex revealed that the roles of TWD40-2 in CME are both distinct from and cooperative with the AP2

158 s (CME), the mechanistic role of Ca(2)(+) in CME remains to be elucidated.

159 is due to an unmet requirement for actin in CME.

160 inery and the membrane, leading to arrest in CME.

161 in maximum height correlated with change in CME and PED volume (r(2) = 0.98 and 0.43, respectively).

162 time monitoring of spatiotemporal changes in CME dynamics and is less prone to errors associated with

163 irect evidence for a molecular checkpoint in CME.

164 he primary role of the actin cytoskeleton in CME is to constrict and elongate the bud neck and drive

165 A role for the F-actin cytoskeleton in CME is well established, and recently, PKA-dependent ass

166 n2, which regulates early and late events in CME in nonneuronal cells.

167 that in uveitic patients, the improvement in CME and inflammation after intravitreal triamcinolone is

168 In addition, improvement in CME associated with uveitis was seen in response to topi

169 tant signaling lipid with conserved roles in CME and actin assembly regulation.

170 receptor internalization and also inhibited CME in primary neurons expressing mutant huntingtin, sho

171 al Initiative on Thrombosis and Cancer (ITAC-CME), established to reduce the global burden of VTE in

172 his Review, we provide an update of the ITAC-CME consensus recommendations based on a systematic revi

173 ved membranes are CME hotspots, and that key CME proteins, clathrin and dynamin, show a strong prefer

174 in core ether (ME) and the carboxymethyl-ME (CME), which exhibit high efficacy in blocking tumor cell

175 llular processes; however, rhomboid-mediated CME regulation has not been described.

176 By monitoring CME of single vesicles in mouse chromaffin cells with ce

177 micromolar range (IC(50): ME 1.5 to 8.2 muM, CME 0.5 to 5 muM).

178 s: (1) CME, (2) IRF without CME, (3) neither CME nor IRF.

179 RF without CME (43.8%) and eyes with neither CME nor IRF (32.5%; P < 0.001).

180 s with IRF without CME and eyes with neither CME nor IRF (52 vs. 60 vs. 66 letters, P < 0.001); highe

181 Non-CME macular cysts in retinal dystrophies can be differen

182 , other membrane-associated proteins and non-CME endocytic protein caveolin1 show no such curvature p

183 to report a case of cystoid macular oedema (CME) associated with Rosai-Dorfman Disease (RDD).

184 suggest that CESA represents a new class of CME cargo proteins and that plant cells might regulate c

185 is necessary for the Ca(2)(+) dependence of CME.

186 Development of CME detected by macular SD OCT during 6 months postopera

187 actors associated with future development of CME included female gender (P = 0.004), increasing tumor

188 om the Sun results in geometric expansion of CME plasma parcels at a speed faster than the local wave

189 supplement can limit or reduce the extent of CME in patients with RP.

190 edema in uveitic patients with a history of CME who underwent phacoemulsification.

191 , the AP2 complex acts as the central hub of CME by docking to the plasma membrane while concomitantl

192 rophylactic treatment to reduce incidence of CME after triple-DMEK surgery.

193 t systems and that ES9 induces inhibition of CME not because of its effect on cellular ATP, but rathe

194 mplicate this mechanism in the inhibition of CME.

195 coded reporters that allow the initiation of CME on demand.

196 Interpretation of CME observations and their interaction with the solar wi

197 coherence of CMEs suggests interpretation of CME observations requires accurate reconstruction of the

198 en made toward elucidating the mechanisms of CME, and the field is becoming increasingly complex, wit

199 incentives to make such integrated models of CME and QI attractive to practitioners.

200 ogeneity in the timing of the early phase of CME, with transient recruitment of 2-4 molecules of dyna

201 namin2 recruitment during the late phases of CME, and promoted dynamin recruitment.

202 ce tomography (OCT) revealed the presence of CME in the left eye.

203 amber and vitreous inflammation, presence of CME, and prior use of regional corticosteroid injections

204 screened for ROP and graded for presence of CME, central foveal thickness (CFT), inner nuclear layer

205 tly express CLCb, exhibit increased rates of CME and altered clathrin-coated pit dynamics.

206 vo systems by demonstrating the reduction of CME dynamics during dorsal closure of Drosophila melanog

207 terior segment inflammation and reduction of CME in pediatric patients with uveitis when used as an a

208 talk between signaling and the regulation of CME, leading to autoregulation of endocytosis and signal

209 cell surface receptors to the regulation of CME.

210 sure high spatial and temporal regulation of CME.

211 Standardized reporting of CME based on OCT may allow for more uniform quantitation

212 e regularity characterized the final 20 s of CME, during which approximately 26 molecules of dynamin2

213 Severity of CME, as assessed by foveal-to-parafoveal thickness ratio

214 analyses to measure discrete early stages of CME and show how sequential, allosterically regulated co

215 TPase dynamin also regulates early stages of CME.

216 which is required to drive multiple steps of CME.

217 al study was pivotal to our understanding of CME and its progression into ever-increasing complexity

218 The results enhance our understanding of CME propagation and shape, which can help to improve spa

219 ics in vivo through a mechanism depending on CME and F-actin remodeling.

220 anipulating PIP(2) synthesis and turnover on CME by quantitative total internal reflection fluorescen

221 on" (SE), an evidence-based method of online CME.

222 ation: 14 offered live and 17 offered online CME courses.

223 these 2 surgical groups for RD (P = 0.19) or CME (P = 1.00).

224 In seedlings of twd40-2-3 and other CME-deficient mutants, a direct correlation was revealed

225 ons, actin dynamics is required to carry out CME successfully.

226 molecular components necessary to carry out CME; however, functional characterization of the compone

227 nd tracking of single fluorescent particles, CME dynamics is not characterized in vivo, so the effect

228 reated patients with CRVO who had persistent CME at month 3.

229 dema (CME) at month 3, those with persistent CME did worse, on average, and significantly so for 0.5

230 asma membrane, where it recruited late-phase CME proteins and supported productive endocytosis, ident

231 RCTs comparing medical strategies to prevent CME after uncomplicated cataract surgery in nondiabetic

232 Prior retinal surgery, history of prior CME.

233 ortant role in development of post-radiation CME.

234 ng whether an iodine supplement could reduce CME in RP.

235 atory drug therapy was effective in reducing CME detected by angiography or optical coherence tomogra

236 Chronic, refractory CME remains a therapeutic challenge, but investigational

237 o better understand mechanisms that regulate CME.

238 f this process, the machinery that regulates CME in plants is largely unknown.

239 form-specific role for dynamin in regulating CME and reveal a feed-forward pathway that could link si

240 There is no uniform method of reporting CME in the literature, which prevents accurate assessmen

241 is maintained in mitotic cells with restored CME, indicating that direct phosphorylation of the CME m

242 Subclinical CME is seen in premature infants; however, CME does not

243 tive week, we observed 9 cases of subsequent CME (12%).

244 As such, CME regulates signaling from cell-surface receptors, but

245 l abilities of these two isoforms to support CME.

246 e this entire complex while still supporting CME.

247 Of ten CME-related proteins we examined, all show preferences f

248 We demonstrate that CME can be 'restarted' in mitotic cells despite high mem

249 Extensive studies have shown that CME proteins actively modulate the plasma membrane curva

250 Thus information cannot propagate across the CME.

251 ent for the actin cytoskeleton to assist the CME machinery to overcome the increased load.

252 1.5 category 1 CME credits by completing the CME quiz that accompanies this issue of In the Clinic.

253 ickness, although higher at baseline for the CME group, was similar at 1 and 2 years follow-up for al

254 The efficacy of educational games for the CME has yet to be established.

255 gests that there may be other causes for the CME seen in this patient population.

256 We show how the CME can be represented in QTT format, then use the expon

257 improvement in VA at follow-up; however, the CME group started and ended with the worst VA among the

258 However, the CME is demonstrated to be channelled during eruption int

259 Yet direct solutions of the CME have remained elusive.

260 ndicating that direct phosphorylation of the CME machinery does not account for shutdown.

261 The AP2 complex of the CME pathway is conserved in yeast, animals, and plants,

262 rcome the infinite dimensional nature of the CME through projections or other means, a common feature

263 are consistent with an ellipse shape of the CME-driven shock provided by the new Ellipse Evolution m

264 alerkin discretization in time to reduce the CME evolution problem to a set of QTT-structured linear

265 ignaling receptors reciprocally regulate the CME machinery remains an open question.

266 Our data reveal that the CME machinery in Arabidopsis is evolutionarily conserved

267 Whereas the CME of constitutively internalized transferrin receptors

268 al-to-parafoveal thickness ratio, within the CME group correlated with poorer cognitive (R2=0.16, P=0

269 These CME models thus share some of the same basic goals as th

270 This CME activity provides expert insight into the Tear Film

271 n addition to regulating cargo entry through CME, Syp1 can promote internalization of Ptr2 through a

272 duce plant defense responses, likely through CME of cell surface-located signaling components.

273 ESA complexes at the plasma membrane through CME.

274 The mechanisms that link NMDAR activation to CME of AMPARs remain elusive.

275 the most abundant adaptor and is pivotal to CME.

276 ent domains contribute to its recruitment to CME sites, site selection, and site maturation.

277 ssing the existing engagement in traditional CME to achieve the goal of equipping practitioners with

278 widely recognized problems with traditional CME.

279 t this cytotoxicity could be abrogated using CME inhibitors or antioxidants, attesting to intracellul

280 articipants with current or resolved uveitic CME.

281 Fifty-six eyes of 42 patients with uveitic CME were prospectively imaged as part of the VISUAL-1 tr

282 t IHCs use dynamin-dependent endocytosis via CME to support vesicle cycling during mild stimulation b

283 of molecules proposed to be internalized via CME, and alters the subcellular enrichment of the early

284 When CME is disrupted, cellular cholesterol pools are instead

285 When CME was inhibited by blocking dynamin action, real-time

286 mum in the first and third patient, in whom CME was the indication for DEX implantation.

287 More eyes with CME (65.3%) developed scarring during 2 years of follow-

288 erapy with difluprednate in 78% of eyes with CME (7/9).

289 In CATT, eyes with CME had worse baseline and follow-up VA, although all gr

290 At baseline, eyes with CME had worse mean VA (letters) than eyes with IRF witho

291 For the eyes with CME, CFT ranged from a geometric mean of 267 microm for

292 th less central foveal swelling in eyes with CME.

293 s lead to the diagnosis of bilateral RP with CME in the right eye.

294 on UIC separately for eyes with and without CME showed a strong inverse significant relationship for

295 ollow-up compared with eyes with IRF without CME (43.8%) and eyes with neither CME nor IRF (32.5%; P

296 mean VA (letters) than eyes with IRF without CME and eyes with neither CME nor IRF (52 vs. 60 vs. 66

297 fluid (IRF) status: (1) CME, (2) IRF without CME, (3) neither CME nor IRF.

298 (8.1%) had CME, 766 (67.7%) had IRF without CME, and 273 (24.1%) had neither.

299 Retinitis pigmentosa with or without CME.

300 Yeast CME requires the proper regulation of actin polymerizati