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

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

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

8 , it is compact and has embedded within it a CCP module (CCP 13) that appears to be highly specialise

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

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

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

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

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

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

15 n increase in CCP size, turnover of abortive CCPs increases, and the rate of CCP maturation decreases

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

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

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

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

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

21 pure chitin preparations, strain TKU012, and CCP.

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

23 t the interaction dynamics between cargo and CCPs.

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

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

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

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

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

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

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

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

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

33 Preclinical positivity for anti-CCP and/or >/=2 RF isotypes was >96% specific for future

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

35 , and this association was specific for anti-CCP-positive RA (OR 7.3, 95% CI 2.7-20.0), but not anti-

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

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

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

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

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

41 e RA (OR 7.3, 95% CI 2.7-20.0), but not anti-CCP-negative RA.

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

43 9-2011), we evaluated the prevalence of anti-CCP positivity among 15,691 (10.2% of 161,808) WHI parti

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

45 further stratified for the presence of anti-CCP, RF, and the PTPN22 risk allele.

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

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

48 1 excluding prednisone) but by 57.5% of anti-CCP-positive women.

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

50 RA, and 15 (2.5%) had IA and RF and/or anti-CCP positivity, suggesting early RA.

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

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

53 s of anti-cyclic citrullinated peptide (anti-CCP) antibodies and current use of biologic agents, but

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

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

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

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

58 and anti-cyclic citrullinated peptide (anti-CCP) antibody testing.

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

60 ody, anti-cyclic citrullinated peptide (anti-CCP) antibody, and rheumatoid factor.

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

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

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

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

65 is specific for a particular RA subset, anti-CCP-positive RA.

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

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

68 1B, was significantly associated in the anti-CCP-positive RA subgroup (P = 4 x 10(-8), OR 0.89), conf

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

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

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

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

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

74 gid and tilted relative to neighbours as are CCPs 12 and 13 with respect to one another.

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

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

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

78 fferences (e.g., cargo and adaptors) between CCPs.

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

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

81 g was associated with the generation of both CCP and RF antibodies (OR 1.7, P = 0.0001).

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

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

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

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

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

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

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

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

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

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

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

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

94 assembly and confirmed that bTfnR-containing CCPs mature more efficiently than bTfnR-free CCPs.

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

96 Ps 10-15 that fit well with scattering data, CCP 14 is folded back onto CCP 13.

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 Its two C-terminal domains (CCP 19-20) anchor fH to self-surfaces where it prevents

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

101 opeptide receptors signal to their enclosing CCPs by ubiquitination.

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

103 compared a recombinant protein encompassing CCP 19-20 with 16 mutants.

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 In one of two arrangements for CCPs 10-15 that fit well with scattering data, CCP 14 is

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

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

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

114 CCPs mature more efficiently than bTfnR-free CCPs.

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

118 days was 87% for HMII alone and 80% for HMII+CCP.

119 in conjunction with HMII implantation (HMII+CCP).

120 8% for the HMII group and 11.3% for the HMII+CCP group.

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

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

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

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

125 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

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

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

128 xpression leads to a progressive increase in CCP size and to the appearance of nonterminal endocytic

129 pressing cells in addition to an increase in CCP size, turnover of abortive CCPs increases, and the r

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

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

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

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

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

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

136 populations there is significant variance in CCP lifetime.

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 By tracking cargo loading in individual CCPs, we found that bTfnR clustering preceded clathrin a

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

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

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

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

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

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

148 t lower cortical tension selectively lowered CCP lifetimes within Fn islands, thus abolishing the spa

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

150 act and has embedded within it a CCP module (CCP 13) that appears to be highly specialised given both

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

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

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

154 ion point/checkpoint mechanism that monitors CCP maturation.

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

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

157 tion and subsequent stabilization of nascent CCPs.

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

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

160 10 but compact and intimate arrangements of CCP 14 with CCPs 12, 13 and 15.

161 its (CCPs) to measure independent aspects of CCP dynamics, including the turnover of abortive and pro

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

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

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

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

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

167 ependently associated with the generation of CCP antibodies (odds ratio [OR] 11.1, P < 0.0001), where

168 ighly dynamic and cargo-responsive nature of CCP assembly and suggest that the observed heterogeneity

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

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

171 of abortive CCPs increases, and the rate of CCP maturation decreases.

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

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

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

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

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

177 -15 and 8-15, implied flexible attachment of CCPs 8 and 9 to CCP 10 but compact and intimate arrangem

178 etween BRIa and BRII with a key component of CCPs, adaptor protein 2.

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

180 Further, disruption of CCPs resulted in increased BRIa aggregation at the cell

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

182 The assembly dynamics of CCPs shows striking heterogeneity.

183 a key source of the differential dynamics of CCPs.

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

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

186 ent affects the initiation and maturation of CCPs is not fully understood.

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

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

189 12, to form a three-dimensional structure of CCPs 10-12 and validated it by small-angle X-ray scatter

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

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

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

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

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

195 scattering data, CCP 14 is folded back onto CCP 13.

196 effects of receptor overexpression on CME or CCP dynamics.

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

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

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

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

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

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

203 reactivity to cyclic citrullinated peptide (CCP).

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

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

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

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

208 m the Center for Computational Pharmacology (CCP) at the University of Colorado School of Medicine.

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

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

211 l imaging of individual clathrin-coated pit (CCP) dynamics has revealed a broad variation in their in

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

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

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

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

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

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

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

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

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

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

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

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

224 etime distributions of clathrin-coated pits (CCPs) to measure independent aspects of CCP dynamics, in

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

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

227 cumulate into maturing clathrin-coated pits (CCPs), whether and how cargo recruitment affects the ini

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

229 BMPRs with proteins in clathrin-coated pits (CCPs).

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

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

232 ding the turnover of abortive and productive CCP species and their relative contributions.

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

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

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

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

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

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

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

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

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

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

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

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

245 e last two of 20 complement control protein (CCP) modules within complement factor H (fH) encompass b

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

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

248 three predicted complement control protein (CCP) modules.

249 actor containing complement control protein (CCP) modules.

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

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

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

253 nd acute production of PI(3,4,5)P(3) shorten CCP lifetime by enhancing the rate of pit maturation, wh

254 One suggestion is that the generally small CCPs 10-15, connected by longer-than-average linkers, ac

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

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

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

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

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

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

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

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

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

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

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

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

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

268 The CCP score was assessed for independent prognostic utilit

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

270 The CCP score was validated to have significant prognostic a

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

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

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

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

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

276 abolishing the spatial heterogeneity in the CCP dynamics.

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

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

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

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

281 Therefore, CCPs seem to function as a negative regulatory membrane

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

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

284 ied CI and CIII as well as autoantibodies to CCP were observed exclusively in patients with AgP and n

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

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

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

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

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

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

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

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

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

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

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.