ライフサイエンスコーパス: CCP

1 CCP with thiol at one end provides the ease of CSGMA fun

2 CCP/CSGMA electrodes were characterized using label-free

3 CCP/CSGMA electrodes were found to be selective against

4 CCPs were typified by their sphericity, small size, and

5 N-BDAN (2D CCP-BD), the bithiophene-based 2D CCP-Th exhibits a wide light-harvesting range (up to 674

6 onding biphenyl-bridged 2D CCP-HATN-BDAN (2D CCP-BD), the bithiophene-based 2D CCP-Th exhibits a wide

7 d with the corresponding biphenyl-bridged 2D CCP-HATN-BDAN (2D CCP-BD), the bithiophene-based 2D CCP-

8 rbon-linked conjugated polymer framework (2D CCP-HATN) has a nitrogen-doped skeleton, a periodical du

9 le (ThDAN) provides the 2D CCP-HATNThDAN (2D CCP-Th).

10 d the robust sp(2) carbon-carbon linkage, 2D CCP-HATN hybridized with carbon nanotubes shows a high c

11 r facilitated charge transfer, which make 2D CCP-Th a promising candidate for PEC water reduction.

12 ng from the shape-persistent framework of 2D CCP-HATN integrated with the electrochemical redox-activ

13 sp(2) -carbon-linked conjugated polymer (2D CCP) is demonstrated.

14 As a result, 2D CCP-Th presents a superb H(2) -evolution photocurrent de

15 -diyl)diacetonitrile (ThDAN) provides the 2D CCP-HATNThDAN (2D CCP-Th).

16 e was calculated as average expression of 31 CCP genes, normalized to 15 housekeeper genes.

17 ry, we examined pre-post outcomes among 3641 CCP clients enrolled before April 2011.

18 by selective engagement of FH, via CCPs 1-4, CCPs 6-8 and CCPs 19-20, with polyanion-rich host surfac

19 lso recognizes the C4 C345C domain through a CCP exosite.

20 d the times that cargo remains confined to a CCP.

21 d dissociation of individual channels with a CCP and, occasionally, their internalization.

22 Chanda, Cook, and Putterman (abbreviated CCP) have now reanalyzed it, taking as a unit of analysi

23 rgo often escapes from a pit before abortive CCP termination or endocytic vesicle production.

24 In contrast, other CCPs (abortive CCPs) are relatively short-lived and disassemble well be

25 otypic clusters, which differentially affect CCP maturation and dynamics.

26 hibition of GSK3beta accelerates CME, alters CCP dynamics and, unexpectedly, increases the rate of CC

27 riates dominated survival analyses, although CCP and hypoxia may inform clinical practice.

28 in the earliest stages of AP2 activation and CCP nucleation.

29 without (TD) the distal leg inhibits CME and CCP dynamics by perturbing clathrin interactions with AP

30 human blood serums with a certified CRP and CCP content.

31 opposite effects on EGFR internalization and CCP dynamics, compared with DGK inhibition.

32 S] score), and a score combining CAPRA-S and CCP was validated.

33 pure chitin preparations, strain TKU012, and CCP.

34 engagement of FH, via CCPs 1-4, CCPs 6-8 and CCPs 19-20, with polyanion-rich host surfaces that bear

35 e verification, we use DASC-resolved ACs and CCPs to quantify CME progression in 11 EAP knockdown con

36 t the interaction dynamics between cargo and CCPs.

37 ], anti-cyclic citrullinated peptide 2 [anti-CCP-2], and RF isotypes), and sera from 99 antibody-nega

38 Among anti-CCP+ RA women, SE alleles were not related to age-adjust

39 s should evaluate SE associations among anti-CCP- adults without RA and potential mechanisms.

40 latives (even those negative for RF and anti-CCP-2) demonstrate reactivity to multiple ACPAs, and the

41 Women with anti-CCP-positive RA and anti-CCP-negative RA had different characteristics with regar

42 that were positive for both antibodies, anti-CCP positivity predated anti-PAD-4 positivity in 9 of 13

43 of probable clinical RA in 2 clinics as anti-CCP positivity or self-reported validated use of disease

44 omen's Health Initiative, classified as anti-CCP+ RA (n = 556) or anti-CCP- non-RA (n = 1,070).

45 s of follow-up, stratifying by baseline anti-CCP status (positive (+) vs. negative (-)).

46 negative DMARD-positive RA and 6.6% for anti-CCP-negative, RF-negative DMARD nonusers).

47 hared epitopes was also much higher for anti-CCP-positive women (18.2%, as opposed to only 5.5% for w

48 an cytokine levels were much higher for anti-CCP-positive/RF-positive women.

49 ated level of any RF isotype and/or IgG anti-CCP antibodies was further associated with an enhanced b

50 e presence of any RF isotype and/or IgG anti-CCP autoantibodies together with an elevated CRP level i

51 In healthy individuals, anti-CCP-producing B cells were also observed more frequently

52 The combined associations of anti-CCP antibody level and biologic agent use with myocardia

53 9-2011), we evaluated the prevalence of anti-CCP positivity among 15,691 (10.2% of 161,808) WHI parti

54 The prevalence of anti-CCP positivity was 8.1%, and the prevalence of RF positi

55 sitive first-degree relatives and 8% of anti-CCP-2- negative first-degree relatives were positive for

56 Fifty-seven percent of anti-CCP-2-positive first-degree relatives and 8% of anti-CCP

57 1 excluding prednisone) but by 57.5% of anti-CCP-positive women.

58 vels, but no associations with hsCRP or anti-CCP levels.

59 classified as anti-CCP+ RA (n = 556) or anti-CCP- non-RA (n = 1,070).

60 for anti-cyclic citrullinated peptide (anti-CCP) antibodies and anti-mycobacterial Hsp65 antibodies.

61 IgG anti-cyclic citrullinated peptide (anti-CCP) antibodies together with an elevated C-reactive pro

62 pes, anti-cyclic citrullinated peptide (anti-CCP) antibodies, 14 cytokines and chemokines (by bead-ba

63 RP), anti-cyclic citrullinated peptide (anti-CCP) antibodies, interleukin-6 (IL-6), and soluble tumor

64 heir anti-cyclic citrullinated peptide (anti-CCP) antibody status, was performed.

65 age, anti-cyclic citrullinated peptide (anti-CCP) antibody titer, disease duration, and C-reactive pr

66 for anti-cyclic citrullinated peptide (anti-CCP), a highly sensitive and specific marker for rheumat

67 s of anti-cyclic citrullinated peptide (anti-CCP), anti-citrullinated vimentin (anti-Cit-vimentin), a

68 itrullinated peptide antibody-positive (anti-CCP+) RA.

69 d baseline specimens, we measured serum anti-CCP, rheumatoid factor (RF), and antinuclear antibody in

70 ectly correlated with the levels of the anti-CCP antibodies, of the Th1/Th17 cytokines, and of the co

71 ated with seropositivity for RF and the anti-CCP antibody, which was highly relevant given the associ

72 1B, was significantly associated in the anti-CCP-positive RA subgroup (P = 4 x 10(-8), OR 0.89), conf

73 iodontitis (56%) than patients who were anti-CCP negative (22%) (P = 0.01).

74 ti-PAD-4 positivity was associated with anti-CCP positivity (odds ratio 5.13 [95% confidence interval

75 set of patients and are associated with anti-CCP positivity.

76 as opposed to only 5.5% for women with anti-CCP-negative DMARD-positive RA and 6.6% for anti-CCP-neg

77 Women with anti-CCP-positive RA and anti-CCP-negative RA had different c

78 NECAP arrival at CCPs parallels that of clathrin and increases with mu2Th

79 rtance of the phosphoinositide metabolism at CCPs in the regulation of insulin signal output.

80 interactions are difficult to study because CCPs display a large degree of lifetime heterogeneity an

81 Associations between CCP score and recurrence were examined, with adjustment

82 to immediate neighbors, but the bend between CCPs 10 and 11 is counter to the arc traced by CCPs 11-1

83 Both CCP and LmP have an extended section of beta structure n

84 st adsorption rate (84%) for PG, followed by CCP, SSP, SPP, alpha-chitin, and beta-chitin.

85 g the complement regulatory domain formed by CCPs 1 to 4.

86 Ps 10 and 11 is counter to the arc traced by CCPs 11-13.

87 tions in C4 and MASP-2 residues at the C345C-CCP interface inhibit the intermolecular interaction and

88 used on the three N-terminal domains (called CCPs or SCRs) of the important complement regulator, hum

89 nes the 6-member cytosolic carboxypeptidase (CCP) family that metabolizes polyglutamate side chain an

90 The cytosolic carboxypeptidases (CCPs) are a subfamily of metalloenzymes within the large

91 We show that without cargo, CCP assembly faces a high energy barrier that is difficu

92 mbinant C4BP mutants, which (i) lack certain CCP domains or (ii) have mutations in single aa as well

93 oited to extract carcinogenic chlorophenols (CCPs) from environmental waters, and a simple and fast m

94 As a consequence, CCPs without cargo are almost always abortive.

95 the rate of CCP maturation, bTfnR-containing CCPs exhibited significantly longer lifetimes than other

96 olved as a key regulatory node to coordinate CCP formation and cargo sorting and ensure high spatial

97 Nonubiquitinated receptors delay CCPs at an intermediate stage of maturation, after clath

98 mutants with additional aa between different CCP domains were used to determine that the binding is m

99 supported by the higher extent of dissolved CCP in serum phase.

100 miscuity in the protein interactions driving CCP maturation than anticipated.

101 lar defects upon knockdown suggest that each CCP may have a function in microtubule modification and

102 opeptide receptors signal to their enclosing CCPs by ubiquitination.

103 To address this question, genes encoding CCPs were identified in the zebrafish genome.

104 port a model in which spores actively engage CCP primarily through BclA interaction with C1q, leading

105 Exposing CCPs 19 and 20 with PspCN and thus enhancing CA on self-

106 We detect no extramitochondrial CCP activity because Ccp1 crosses the outer mitochondria

107 Unrestricted availability of FH CCPs 19-20 and an optimal spatial orientation between th

108 e more B cells with autoimmune potential for CCP than those without such HLA alleles (odds ratio 8.1,

109 rtner of endocytic proteins, is required for CCP assembly, but little is currently known about its co

110 structure yielded an S-shaped structure for CCPs 10-13 in which modules are tilted by 80-110 degrees

111 oltage-gated potassium channels into forming CCPs in living cells.

112 Furthermore, by composing a four-CCP DAF-MCP chimera with robust CFA (for C3b and C4b) an

113 We show that in a four-CCP framework, a functional unit for each of the regulat

114 Including this four-CCP structure in interpretation of scattering data for t

115 of putative PfRh4-interacting residues from CCP 1 into their homologous positions within CCP 8; stri

116 factors are likely cleaved C-terminally from CCP tandems, suggesting that not only domain architectur

117 assification (DASC)", that resolves ACs from CCPs based on single channel fluorescent movies.

118 tiparasitic treatment on CD8(+) T cells from CCPs with asymptomatic clinical forms of disease.

119 ant for its targeting to nascent and growing CCPs, whereas the membrane-binding and curvature-generat

120 eveal that up to four consecutive homologous CCP domains (i-iv), responsible for inhibition, bind in

121 Data mining indicates that most human CCP-containing factors are likely cleaved C-terminally f

122 In CCP, Trp(191) forms a stable cationic radical after reac

123 Trp residue, Trp(208) in LmP and Trp(191) in CCP, that is situated adjacent to the proximal His heme

124 zard ratio for a 1-unit change [doubling] in CCP 1.89; 95% CI 1.54-2.31; p=5.6x10(-9)) and the best m

125 y one source of the large heterogeneities in CCP dynamics and provide a mechanism for the anomalous d

126 hazard ratio (HR) for each unit increase in CCP score (range, -1.62 to 2.16) was 2.1 (95% CI, 1.6 to

127 emain as to the molecular events involved in CCP initiation, stabilization, and curvature generation.

128 sured the expression of 31 genes involved in CCP with quantitative RT-PCR on RNA extracted from forma

129 adjacent to the proximal His heme ligand in CCP, APX, and LmP.

130 er affinity for PfRh4 than the native one in CCP 1.

131 rovides stability to the Trp(191) radical in CCP.

132 -based temporal regulatory system results in CCP maturation being delayed and/or stalled, hence impai

133 that monitor the fidelity of early stages in CCP maturation.

134 mational changes relate to distinct steps in CCP formation in living cells remains unknown.

135 populations there is significant variance in CCP lifetime.

136 ensitive detector of phenotypic variation in CCP dynamics that is uncorrelated to the variation in bi

137 Large sequence variations in CCP domains explain the diverse C3b-binding patterns, wi

138 y receptors, and functionality of T cells in CCPs, PBMCs were isolated.

139 These findings suggest that, in CCPs, antiparasitic treatment improved the quality of Ag

140 how that local clustering of bTfnR increased CCP initiation.

141 variations in EAP association to individual CCPs and the resulting variations in maturation.

142 ng that baggage, AJR emphasize institutions, CCP emphasize social capital, and I identify many differ

143 The role of intervening CCPs 9-18 in this process is obscured by lack of structu

144 d it controls specific receptor loading into CCPs by sensing when a sufficient quorum is reached.

145 The aHUS-linked CCP 19 mutant D1119G-CFH had virtually no CA on (self-li

146 The aHUS-linked CCP 20 mutant S1191L/V1197A-CFH (LA-CFH) had dramaticall

147 sted that at least four of the six mammalian CCPs function as tubulin deglutamylases.

148 ining 20 complement-control protein modules (CCPs 1-20), may be compromised by disease-linked mutatio

149 terminal complement control protein modules (CCPs 1-3) of CR1, which intriguingly also accommodate bi

150 ng of 20 complement control protein modules (CCPs), and its splice product FH-like protein 1 (FHL-1;

151 Whereas most CCPs catalyze hydrolysis of alpha-carboxyl-linked glutam

152 Nearly half of nascent CCPs abort, whereas others are stabilized by unknown mec

153 tion and subsequent stabilization of nascent CCPs.

154 ays an important role in stabilizing nascent CCPs.

155 ing Cit-fibrinogen and Cit-vimentin, but not CCP-2, were associated with an increased aortic plaque b

156 equently, the catalase activity of Cta1, not CCP activity, contributes to mitochondrial H2O2 detoxifi

157 10 but compact and intimate arrangements of CCP 14 with CCPs 12, 13 and 15.

158 the lifetimes of dynamin, a key component of CCP scission.

159 hrin structures, indicating broad control of CCP assembly by Ca(2+) signals.

160 mong orthologues, a structural dependency of CCP 14 on its neighbors is suggested; this has implicati

161 to "necked"/"closed" CCVs and a doubling of CCP/CCV diameter, whereas AP2 depletion has opposite eff

162 itiation and controls the rate and extent of CCP growth.

163 CCPs and show that the stochastic nature of CCP assembly plays a crucial role in causing their obser

164 ics and, unexpectedly, increases the rate of CCP initiation.

165 changes in cargo loading altered the rate of CCP maturation, bTfnR-containing CCPs exhibited signific

166 rn, NECAP recruits drivers of late stages of CCP formation, including SNX9, via a site distinct from

167 ns and their adaptors during early stages of CCP nucleation and stabilization and highlight the impor

168 s 13-14 and 14-15, the aberrant structure of CCP 13 and the variability of 13-14 linker sequences amo

169 subgroups, and in 89% (EiC) and 75% (VLS) of CCP agencies.

170 s CFH tightly and increases accessibility of CCPs 19 and 20.

171 ion to control of initiation and assembly of CCPs, EGF stimulation also elicited a Ca(2+)- and PKC-de

172 -15 and 8-15, implied flexible attachment of CCPs 8 and 9 to CCP 10 but compact and intimate arrangem

173 duct FH-like protein 1 (FHL-1; consisting of CCPs 1-7) are major regulators of the alternative pathwa

174 d signaling receptor, delays the dynamics of CCPs in which it is localized.

175 The assembly dynamics of CCPs shows striking heterogeneity.

176 a key source of the differential dynamics of CCPs.

177 ks these observations with the energetics of CCPs and kinetics of their assembly.

178 diated endocytosis of EGFR, the formation of CCPs harboring EGFR, and EGFR signaling.

179 erently, p.R522H slows down the formation of CCPs without affecting their internalization.

180 and significantly increases the lifetime of CCPs.

181 67 EAPs throughout the maturation process of CCPs.

182 wn about such "cargo-mediated regulation" of CCPs by signaling receptors.

183 d visualized it with a solution structure of CCPs 1-3 derived by NMR and small angle x-ray scattering

184 12, to form a three-dimensional structure of CCPs 10-12 and validated it by small-angle X-ray scatter

185 gnals to facilitate formation of a subset of CCPs, thus modulating its own signaling and endocytosis.

186 The results showed that treatment of CCPs with the asymptomatic form of the disease induces a

187 his provides evidence for the versatility of CCPs to control diverse cellular processes.

188 ruitment to CCPs and their direct effects on CCP dynamics.

189 tution mutagenesis the PfRh4-binding site on CCP 1 and visualized it with a solution structure of CCP

190 In contrast, other CCPs (abortive CCPs) are relatively short-lived and disa

191 ed significantly longer lifetimes than other CCPs within the same cell.

192 fication and ciliary function and that other CCPs are not able to compensate for the loss of one.

193 ivation of the classical complement pathway (CCP) was a primary mechanism for spore phagocytosis.

194 Chronic chagasic patients (CCPs) have dysfunctional CD8(+) T cells that are charact

195 e for the anti-cyclic citrullinated peptide (CCP) antibodies were more likely to have moderate to sev

196 reactivity to cyclic citrullinated peptide (CCP).

197 yer of thiol terminated coiled-coil peptide (CCP) linked together by the thrombin specific cleavage s

198 c) citrullinated filaggrin-derived peptides (CCP).

199 istic of both yeast cytochrome c peroxidase (CCP) and plant cytosolic ascorbate peroxidase (APX).

200 rystal structure of cytochrome c peroxidase (CCP) compound I (CmpI) using data obtained with the Stan

201 observe the dynamics of clathrin-coated pit (CCP) assembly in real time.

202 mplexes, which initiate clathrin-coated pit (CCP) assembly, are activated by conformational changes i

203 Analysis of clathrin-coated pit (CCP) dynamics led us to propose the existence of a rate-

204 uantitative analysis of clathrin-coated pit (CCP) dynamics, we have evaluated the differential functi

205 to a decreased rate of clathrin-coated pit (CCP) initiation and increased lifetimes of productive CC

206 ion event starts during clathrin-coated pit (CCP) initiation and increases throughout CCP lifetime.

207 docytic cargoes control clathrin-coated pit (CCP) maturation, but it is not known how such regulation

208 olecules into a growing clathrin-coated pit (CCP).

209 s via the formation of clathrin-coated pits (CCPs) at the plasma membrane, which invaginate to form c

210 hology and kinetics of clathrin-coated pits (CCPs) by directly following their dynamics of formation,

211 Clathrin-coated pits (CCPs) in proximity to substrate contacts exhibit slower

212 mbly and maturation of clathrin-coated pits (CCPs) into cargo-containing vesicles.

213 s (ACs) from bona fide clathrin-coated pits (CCPs) is required but unaccomplished.

214 ntly, Lpd localizes to clathrin-coated pits (CCPs) just before vesicle scission and regulates vesicle

215 erogeneous dynamics of clathrin-coated pits (CCPs) might be the different cargo content.

216 d growth/maturation of clathrin-coated pits (CCPs) that eventually pinch off and internalize as clath

217 rs via the assembly of clathrin-coated pits (CCPs) that invaginate and pinch off to form clathrin-coa

218 lating the dynamics of clathrin-coated pits (CCPs) that mediate their internalization.

219 plasma membrane termed clathrin-coated pits (CCPs) that mediate vesicle formation.

220 in the ratio of "open" clathrin-coated pits (CCPs) to "necked"/"closed" CCVs and a doubling of CCP/CC

221 centrated at endocytic clathrin-coated pits (CCPs) via interactions with the scaffold protein interse

222 ed by the formation of clathrin-coated pits (CCPs), in which adaptors nucleate clathrin assembly.

223 n-coated vesicles from clathrin-coated pits (CCPs).

224 s and clathrin to form clathrin-coated pits (CCPs).

225 water-soluble cationic conjugated polymers (CCPs), poly(phenylene ethynylene) (PPE) derivatives, are

226 hitinous materials of cicada casting powder (CCP), shrimp shell powder (SSP), squid pen powder (SPP),

227 Some CCPs are long-lived (productive CCPs); they bind cargo and grow in size to form clathrin

228 We also estimate the lifetimes of productive CCPs and show that the stochastic nature of CCP assembly

229 iation and increased lifetimes of productive CCPs, as determined by quantitative live-cell total inte

230 White Part A HIV Care Coordination Program (CCP), launched at 28 agencies in 2009, applies multiple

231 Cell cycle progression (CCP) increased with sequential inactivation of tumor sup

232 alue of a predefined cell cycle progression (CCP) score in two cohorts of patients with prostate canc

233 k score, denoted the cell-cycle progression (CCP) score, in predicting contemporary radical prostatec

234 ion in the analysis of cytochrome c protein (CCP) and C-reactive protein (CRP (with less side interfe

235 e C-terminal domain-like carotenoid protein (CCP).

236 Indeed, the complement control protein (CCP) 8 domain of C4BP, which would otherwise be sterical

237 dentified on the complement control protein (CCP) domain 1/CCP2 and CCP8 of the C4BP alpha-chains.

238 sed to show that complement control protein (CCP) domains 8 and 2 of the alpha-chain were responsible

239 (comprising two complement control protein (CCP) domains and the serine protease (SP) domain).

240 sed of repeating complement control protein (CCP) domains where two to four successive domains contri

241 which consist of complement control protein (CCP) domains, similarly to the immunomodulatory HpARI an

242 s composed of 30 complement control protein (CCP) modules, organized into four long homologous repeat

243 h consists of 20 complement control protein (CCP) modules, protects self-tissue but not foreign organ

244 actor containing complement control protein (CCP) modules.

245 three predicted complement control protein (CCP) modules.

246 C-terminal domain-like carotenoid proteins (CCPs).

247 lution structures of overlapping recombinant CCP pairs, 10-11 and 11-12, to form a three-dimensional

248 and low-risk subset; the combined CAPRA-S + CCP score consistently predicted outcomes across the ran

249 ng data for the longer recombinant segments, CCPs 10-15 and 8-15, implied flexible attachment of CCPs

250 ollectively, our SICM-FCM findings at single CCP level, backed up by electron microscopy data, argue

251 cture with CCP 12 from the previously solved CCP 12-13 structure yielded an S-shaped structure for CC

252 Some CCPs are long-lived (productive CCPs); they bind cargo a

253 mechanism by which cargo binding stabilizes CCPs and facilitates their growth.

254 activities is formed by only two successive CCPs wherein each participates in the function, albeit C

255 Superimposing CCP 12 of this 10-12 structure with CCP 12 from the prev

256 ) and also to nuclear DNA via its N-terminal CCP module pair (CCP1/2), tethering active IL-33 within

257 g of a ligand-binding site in the C-terminal CCPs 19-20 that is cryptic in full-length native FH.

258 It has long been assumed that CCP activity detoxifies mitochondrial H2O2 because of th

259 urface plasmon resonance to demonstrate that CCP 1 contains all the critical residues for PfRh4 inter

260 mon trafficking components and indicate that CCP regulation by signaling receptors can operate via di

261 Results reveal that CCP/CSGMA electrodes have a limit of detection (LOD) of

262 , named decay cofactor protein, we show that CCP functional units can be linked to design a dual-acti

263 Consistent with this, we show that CCP size and dynamic behavior varies with low density li

264 We conclude that CCPs 19 and 20 are critical for efficient CA on self-sur

265 Live microscopy demonstrated that CCPs are short lived and culminate in a peak of dynamin

266 The CCP score was assessed for independent prognostic utilit

267 The CCP score was calculated as average expression of 31 CCP

268 The CCP score was validated to have significant prognostic a

269 ive model (final multivariate analysis), the CCP score and prostate-specific antigen (PSA) concentrat

270 Epsin1 detects the signal at the CCP and is required for ubiquitin-promoted scission.

271 In the TURP cohort, the CCP score was the most important variable for prediction

272 Combining the CCP and CAPRA-S improved the concordance index for both

273 Heterogeneity in the hazard ratio for the CCP score was not noted in any case for any clinical var

274 After prostatectomy, the CCP score was useful for predicting biochemical recurren

275 We suggest that the CCP and its homologs constitute a new family of caroteno

276 this study provide strong evidence that the CCP score is a robust prognostic marker, which, after ad

277 In MASP-2, an exosite located within the CCP domains recognizes the C4 C345C domain 60 A from the

278 d highlight the importance of GAK throughout CCP maturation that is consistent with GAK's multifuncti

279 it (CCP) initiation and increases throughout CCP lifetime.

280 Thus, CCP/CSGMA electrodes provide high specificity toward thr

281 plied flexible attachment of CCPs 8 and 9 to CCP 10 but compact and intimate arrangements of CCP 14 w

282 hrough BclA interaction with C1q, leading to CCP activation and opsonophagocytosis of spores in an Ig

283 bits an intense and stable signal similar to CCP Compound I.

284 ding times of cargo molecules associating to CCPs are much shorter than the overall endocytic process

285 However, most EAPs bind to CCPs in low numbers, making the measurement of EAP assoc

286 cts exhibit slower dynamics in comparison to CCPs found more distant from adhesions.

287 itol phosphatase synaptojanin 1 localizes to CCPs and controls early stabilization and maturation eff

288 Clathrin is recruited to CCPs through interactions between the AP2 complex and it

289 r unbiased measurement of EAP recruitment to CCPs and their direct effects on CCP dynamics.

290 eves this inhibition, effectively triggering CCP scission and producing a receptor-containing endocyt

291 A single carotenoid molecule spans the two CCPs in the dimer.

292 achieved by selective engagement of FH, via CCPs 1-4, CCPs 6-8 and CCPs 19-20, with polyanion-rich h

293 Reversals of fortune disappeared when CCP analyzed populations rather than geographic regions:

294 ere prospectively captured by the ISARIC WHO CCP study.

295 imposing CCP 12 of this 10-12 structure with CCP 12 from the previously solved CCP 12-13 structure yi

296 act and intimate arrangements of CCP 14 with CCPs 12, 13 and 15.

297 CCP 1 into their homologous positions within CCP 8; strikingly, this engineered binding site had an a

298 ling is regulated by its accumulation within CCPs.

299 phosphate-5-kinase cannot be detected within CCPs but functions in initiation and controls the rate a

300 lasma membrane and its local turnover within CCPs control multiple stages of CCV formation.