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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
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
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
14 We define molecular mechanisms for adaptive CME in cancer cells and a role for the reciprocal crosst
16 cells contributes to a program of "adaptive" CME that alters signaling to enhance cancer cell surviva
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
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
27 ind that the positively curved membranes are CME hotspots, and that key CME proteins, clathrin and dy
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
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
36 s near Earth and Mars confirm the channelled CME motion, and are consistent with an ellipse shape of
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
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
55 lymerization promotes vesicle fission during CME by inducing cholesterol-dependent membrane reorganiz
58 that the dynamics of vesicle fission during CME is Ca(2)(+) dependent but becomes Ca(2)(+) independe
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
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
74 ations, resolution of cystoid macular edema (CME), and anterior chamber and vitreous inflammation wer
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
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
85 rocesses like clathrin-mediated endocytosis (CME) across a diverse range of organisms and mechanical
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
92 erstanding of clathrin-mediated endocytosis (CME) dynamics is based on detection and tracking of fluo
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
102 membrane via clathrin-mediated endocytosis (CME) is a key mechanism for regulating synaptic strength
105 eurons, where clathrin-mediated endocytosis (CME) is dramatically impaired, to gain insight into the
107 we find that clathrin-mediated endocytosis (CME) is harnessed by enteroviruses to traffic cholestero
109 in the brain, clathrin-mediated endocytosis (CME) is the dominant mode of synaptic vesicle retrieval
117 ed either via clathrin-mediated endocytosis (CME) or independently of clathrin (CIE) remains segregat
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
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
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
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
146 y) had a significantly higher rate of future CME (n = 66; 50%) compared with eyes without subclinical
148 ining CME and IRF at baseline, 92 (8.1%) had CME, 766 (67.7%) had IRF without CME, and 273 (24.1%) ha
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
157 omplex revealed that the roles of TWD40-2 in CME are both distinct from and cooperative with the AP2
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
164 he primary role of the actin cytoskeleton in CME is to constrict and elongate the bud neck and drive
167 that in uveitic patients, the improvement in CME and inflammation after intravitreal triamcinolone is
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
180 s with IRF without CME and eyes with neither CME nor IRF (52 vs. 60 vs. 66 letters, P < 0.001); highe
182 , other membrane-associated proteins and non-CME endocytic protein caveolin1 show no such curvature p
184 suggest that CESA represents a new class of CME cargo proteins and that plant cells might regulate c
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
191 , the AP2 complex acts as the central hub of CME by docking to the plasma membrane while concomitantl
193 t systems and that ES9 induces inhibition of CME not because of its effect on cellular ATP, but rathe
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
200 ogeneity in the timing of the early phase of CME, with transient recruitment of 2-4 molecules of dyna
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
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
212 e regularity characterized the final 20 s of CME, during which approximately 26 molecules of dynamin2
214 analyses to measure discrete early stages of CME and show how sequential, allosterically regulated co
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
220 anipulating PIP(2) synthesis and turnover on CME by quantitative total internal reflection fluorescen
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
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
235 atory drug therapy was effective in reducing CME detected by angiography or optical coherence tomogra
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
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
257 improvement in VA at follow-up; however, the CME group started and ended with the worst VA among the
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
268 al-to-parafoveal thickness ratio, within the CME group correlated with poorer cognitive (R2=0.16, P=0
271 n addition to regulating cargo entry through CME, Syp1 can promote internalization of Ptr2 through a
277 ssing the existing engagement in traditional CME to achieve the goal of equipping practitioners with
279 t this cytotoxicity could be abrogated using CME inhibitors or antioxidants, attesting to intracellul
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
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
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