ライフサイエンスコーパス: CTF

1 CTF identifies robust patterns in sparse compositional d

2 CTF-eta generation is mediated in part by membrane-bound

3 CTF-induced apoptosis is transcription dependent and med

4 CTF-induced stabilization of p53 is sensitive to the MEK

5 CTFs and Abeta(21-30) had a high binding propensity to t

6 CTFs co-assembled with Abeta(1-42) into large heteroolig

7 CTFs containing RRM2 generated from de novo cleavage of

8 CTFs produced by eta-secretase are enriched in dystrophi

9 CTFs synthesised their own collagen matrix in fibrin-bas

10 ia, TF-OCM is well-suited to the study of 3D CTF dynamics, and may prove advantageous for the study o

11 enable the quantitative reconstruction of 3D CTFs in scattering media with minute-scale temporal samp

12 ycycline-suppressible expression of a TDP-43 CTF (amino acids 208-414, designated 208 TDP-43 CTF), pr

13 Importantly, 208 TDP-43 CTF and phosphorylated TDP-43 were rapidly cleared when

14 Thus, our results show that TDP-43 CTF expression recapitulates key biochemical features of

15 demonstrate that Camk2a-directed 208 TDP-43 CTF overexpression is sufficient to cause hippocampal pa

16 age site, Arg(208), of a pathological TDP-43 CTF purified from FTLD-U brains and show that the expres

17 P-43 Tg mice, detergent-insoluble 208 TDP-43 CTF was present in a diffuse punctate pattern in neurona

18 (amino acids 208-414, designated 208 TDP-43 CTF), previously identified in FTLD-TDP brains.

19 that the expression of this and other TDP-43 CTFs in cultured cells recapitulates key features of TDP

20 n vivo, suggesting an active role for TDP-43 CTFs in the pathogenesis of FTLD-TDP and related TDP-43

21 the hypothesis that the generation of TDP-43 CTFs is an important step in the pathogenesis of FTLD-U

22 nctional consequences of pathological TDP-43 CTFs remained unknown.

23 s in a cell culture system expressing TDP-43 CTFs, and this is significant because the regulation of

24 of the physical characteristics that affect CTF activity and advance our ability to design, synthesi

25 PP from both alpha-secretase cleavage (alpha-CTF, named C83 according to its band size) and BACE1 cle

26 e of the alpha-COOH-terminal fragment (alpha-CTF) of APP and corresponding elevation of the NH(2)-ter

27 of APP [for alpha-C-terminal fragment (alpha-CTF), 54% and p = 0.04; for beta-CTF, 35% and p = 0.03].

28 ctive ADAM10 correlates with increased alpha-CTF cleavage, and elevated sAPP-alpha.

29 e meprin beta, the levels of the alternative CTF decreased and the CTF ratio was restored back to APP

30 in addition to the long-known CTF-alpha and CTF-beta fragments generated by the alpha- and beta-secr

31 APP, beta-secretase, beta-amyloid, and CTF were significantly increased in type 2 diabetic rats

32 d induction of A beta peptide generation and CTF-gamma cleavage product formation.

33 On the plasma membrane, NTF and CTF behave as separate membrane proteins involved, respe

34 However, separated NTF and CTF can re-associate on solubilisation.

35 stigated the interaction between Abeta42 and CTFs using photoinduced cross-linking and dynamic light

36 S1P-lyase impairs the degradation of APP and CTFs in lysosomal compartments and also decreases the ac

37 estingly, the strong accumulation of APP and CTFs in S1P-lyase-deficient cells was reversed by select

38 cretase, cleave Cad6B to produce the NTF and CTFs previously observed in vivo.

39 These results indicate that the NTFs and CTFs are recruited to distinct transport pathways and re

40 e processed into differently tagged NTFs and CTFs that reveal distinct distributions and characterist

41 a into N- and C-terminal fragments (NTFs and CTFs), which then target independently of each other to

42 This APP CTF degradation phase was accompanied by sustained accum

43 APP CTFs that accumulate in cells lacking gamma-secretase ac

44 ta indicate that the levels of flAPP and APP CTFs associated with exosomes mirror the cellular levels

45 secretion of full-length APP (flAPP) and APP CTFs via the exosome secretory pathway in vivo.

46 , and enzymes that cleave both flAPP and APP CTFs were identified in brain exosomes.

47 Although higher levels of both flAPP and APP CTFs were observed in exosomes isolated from the brains

48 mirror the cellular levels of flAPP and APP CTFs.

49 flAPP, APP CTFs, and enzymes that cleave both flAPP and APP CTFs we

50 cessing of certain substrates, including APP CTFs, while limiting processing of other potential subst

51 specific releasing system of neurotoxic APP CTFs and Abeta, but the secretion of exosomes enriched w

52 group II mGluR agonist DCG-IV, levels of APP CTFs in the synaptoneurosomes initially increased but th

53 solation studies indicate recruitment of APP CTFs into cholesterol- and sphingolipid-rich lipid rafts

54 Enhanced degradation of APP CTFs was selective because no such effects were obtained

55 id-rich lipid rafts, and co-residence of APP CTFs, PS1, and syntaxin 6 in DIM patches derived from th

56 576 and wild-type mice are enriched with APP CTFs relative to flAPP.

57 the secretion of exosomes enriched with APP CTFs, neurotoxic proteins that are also a source of secr

58 Remarkably, unlike the case of APP, CTFs derived from Notch1, Jagged2, deleted in colorectal

59 APP-CTF accumulation initiates CREB signaling cascade throug

60 rent EC(50) of approximately 10 muM) and APP-CTF (apparent EC(50) of approximately 20 muM) in a gamma

61 ficant accumulation of Abeta peptide and APP-CTF and diminished the effect of SMER28.

62 anges in APP subcellular trafficking and APP-CTF degradation.

63 involved in the degradation of Abeta and APP-CTF, and Atg5 was necessary for the effect of SMER28.

64 autophagy in the clearance of Abeta and APP-CTF.

65 abnormal APP processing and Abeta42/C99/APP-CTF deposition.

66 je cells, where it co-localized with C99/APP-CTF.

67 precursor protein (APP)-derived fragment APP-CTF levels in cell lines and primary neuronal cultures.

68 sor protein cleaved C-terminal fragment (APP-CTF) degradation and amyloid beta clearance in an Atg5-d

69 ursor protein carboxy-terminal fragment (APP-CTF).

70 f APP intracellular C-terminal fragment (APP-CTF).

71 t C99 or other APP C-terminal fragments (APP-CTF), but not Abeta42, accumulated in Purkinje cells, ma

72 RNAi silencing of Fe65 increased APP-CTF levels, although also decreasing Abeta levels in H4-

73 The level of the 25-kDa APP-CTF was evaluated in three independent CSF sample sets o

74 ckdown of AP2 reduced autophagy-mediated APP-CTF degradation.

75 ch autophagy mediates the degradation of APP-CTF and the clearance of amyloid beta.

76 lopamine treatment decreases the rate of APP-CTF degradation.

77 ptor for the recognition and shipment of APP-CTF from the endocytic pathway to the LC3-marked autopha

78 -mediated processing of a larger pool of APP-CTF on the endosomal membrane.

79 naling cascade through an association of APP-CTF with Galphas protein.

80 hat AP2 regulated the cellular levels of APP-CTF.

81 tion with the gamma-secretase substrate, APP-CTF.

82 Our data suggest that APP-CTF could be a potential diagnostic biomarker for AD.

83 An RNA interference screen using APP-CTF [99-residue CTF (C99)]- and Notch-specific gamma-sec

84 that AP2 and PICALM cross-link LC3 with APP-CTF.

85 ight chain 3-II cocompartmentalized with APP-CTF.

86 intraneuronal accumulation of oAbeta and APP-CTFs and resultant lysosomal pathology at early stages o

87 Furthermore, alpha-synuclein and APP-CTFs and/or Abeta were found to accumulate in different

88 resulted in the accumulation of APP and APP-CTFs in the ERC in addition to the cell surface.

89 the levels of APP-C-terminal fragments (APP-CTFs) and Abeta in H4 human neuroglioma cells stably ove

90 ation of APP carboxylterminal fragments (APP-CTFs) and oligomeric amyloid beta (oAbeta) but no histol

91 precursor protein C-terminal fragments (APP-CTFs) and/or Abeta.

92 amilial Alzheimer's disease mutations in APP-CTFs did not affect endocytic recycling of these protein

93 Instead, cyclopamine redirects APP-CTFs to the lysosome.

94 We demonstrate that APP-CTFs are detectable in human CSF, being the most abundan

95 -terminal fragment (CTF), which promoted APP/CTF ubiquitination.

96 ess this question, we used a fully atomistic CTF model to test both Ca(2+) binding strength and the e

97 lution ( approximately 1mum) of the LC based CTF transducer, a wide range of CTFs was determined (10-

98 nts 2 and 3 established that these EEG-based CTFs are contingent on the voluntary storage goals of th

99 n mnemonic precision, showing that EEG-based CTFs provide a sensitive measure of the quality of senso

100 Critically, these EEG-based CTFs were robust predictors of both between- and within-

101 F-deformations was then applied in a bespoke CTF mapping software to estimate CTFs and to map CTF fie

102 beta-CTF alone induced atrophy of BFCNs that was rescued by t

103 e full-length wild-type APP (APPWT) and beta-CTF both induced endosomal enlargement and disrupted NGF

104 oEr2 coprecipitated with APP alpha- and beta-CTF, and F-spondin reduced the levels of APP intracellul

105 P and increases Abeta secretion and APP beta-CTF (C-terminal fragment) generation by promoting BACE1-

106 The reduction in APP beta-CTF was blocked by receptor-associated protein (RAP), an

107 C99 (also known as beta-CTF) is the 99 residue transmembrane C-terminal domain (

108 g to its band size) and BACE1 cleavage (beta-CTF/C99).

109 ment (alpha-CTF), 54% and p = 0.04; for beta-CTF, 35% and p = 0.03].

110 (APP) and its beta-C-terminal fragment (beta-CTF) act though increased activation of Rab5 to cause en

111 eavage of the beta C-terminal fragment (beta-CTF) from the Abeta precursor protein, the gamma-secreta

112 Therefore, increased APP and/or beta-CTF impact the endocytic pathway to disrupt NGF traffick

113 stem and support mounting evidence that beta-CTF may be critical in AD pathogenesis.

114 within the transmembrane domain of the beta-CTF (also referred to as C99) increases the ratio betwee

115 al domains, decreased production of the beta-CTF of APP and Abeta in transfected cells and primary ne

116 eady-state levels of APP and alpha- and beta-CTFs, and attenuated Abeta generation by accelerating fl

117 fects on APP beta C-terminal fragments (beta-CTFs), which accumulate in all mutant neurons.

118 unction correlated with accumulation of beta-CTFs, not Abeta, and could be rescued by pharmacological

119 or treatment also increased endogenous beta2-CTF levels in neuroblastoma cells and mouse primary neur

120 remaining 15-kDa C-terminal fragment (beta2-CTF) was independently inhibited by three specific gamma

121 e DAPT treatment resulted in increased beta2-CTF levels, we also tested whether beta2-CTFs or beta2-I

122 d gamma-secretase mediated cleavage of beta2-CTF is required for cell-cell adhesion and migration of

123 Interestingly, elevated levels of beta2-CTFs, but not ICDs, also blocked cell migration by 81 to

124 ta2-CTF levels, we also tested whether beta2-CTFs or beta2-ICDs would directly affect cell migration

125 st particular domains served to characterize CTFs of APP in human CSF.

126 ts that the amount of beta-secretase cleaved CTFs (betaCTFs) of APP underlies these transport differe

127 Herein we report a new strategy to construct CTFs (CTF-HUSTs) via a polycondensation approach, which

128 demonstrate that distinct parameters control CTF inhibition of Abeta42 assembly and Abeta42-induced t

129 Herein, the synthesis of highly crystalline CTFs via directly controlling the monomer feeding rate i

130 we report a new strategy to construct CTFs (CTF-HUSTs) via a polycondensation approach, which allows

131 Comparison to Abeta40-derived CTFs showed that the C-terminal dipeptide I41-A42 strong

132 bilizing the beta-hairpin in Abeta42-derived CTFs.

133 sight into the mechanisms by which different CTFs inhibit the toxic effect of Abeta42 and suggest tha

134 After shedding of this ectodomain, CTF-eta is further processed by ADAM10 and BACE1 to rele

135 assembly in the presence of three effective CTF inhibitors and an ineffective fragment, Abeta(21-30)

136 owing the rapid cleavage of p115, endogenous CTF translocated to the cell nucleus and its nuclear imp

137 n a bespoke CTF mapping software to estimate CTFs and to map CTF fields.

138 toxin and a cytosolic translocation factor (CTF) complex.

139 on tool, compositional tensor factorization (CTF), that incorporates information from the same host a

140 Here we compared chick tendon fibroblasts (CTFs) at three stages of embryonic development with CTFs

141 ssociation within the cardiac thin filament (CTF) is a fundamental regulator of normal contraction an

142 in biosynthesis and cotranslational folding (CTF).

143 was to develop a novel cell traction force (CTF) transducer system based on cholesteryl ester liquid

144 Cellular traction forces (CTFs) play an integral role in both physiological proces

145 ely expressing the C-terminal KSR1 fragment (CTF-KSR1).

146 tly associated with the C-terminal fragment (CTF) but also a novel (Pc1) form (Pc1(deN)) in which NTF

147 on of APP and its carboxy-terminal fragment (CTF) by activation of the lysosomal/autophagy pathway.

148 sequent decrease in APP C-terminal fragment (CTF) content in secreted exosomes, but had minimal effec

149 e treatment reduced APP-C-terminal fragment (CTF) delivery to the trans-Golgi network where gamma-sec

150 f an alternative larger C-terminal fragment (CTF) increased in the APP-S675E cells, whereas the CTF f

151 E1 activities increased C-terminal fragment (CTF) levels of KCNE1 and 2 in human embryonic kidney (HE

152 se cleavage generates a C-terminal fragment (CTF) of 205 residues.

153 l coactivator of the COOH-terminal fragment (CTF) of ErbB-4.

154 120 kDa membrane-bound C-terminal fragment (CTF) of LDLR had reduced capacity to bind LDL and when e

155 The C-terminal fragment (CTF) of TREM2 generated by ectodomain shedding is cleave

156 n of its 205 amino acid C-terminal fragment (CTF) precedes observable Golgi fragmentation.

157 etase, beta-amyloid, COOH-terminal fragment (CTF), insulin receptor, IGF-1 receptor, glycogen synthas

158 , membrane bound carboxyl terminal fragment (CTF), levels of beta-amyloid (Abeta) peptides and select

159 APP specifically at its C-terminal fragment (CTF), which promoted APP/CTF ubiquitination.

160 the generation of brain C-terminal fragment (CTF)-gamma cleavage product of amyloid precursor protein

161 ransmembrane-containing C-terminal fragment (CTF).

162 study assesses whether C-terminal fragments (CTF) of the amyloid precursor protein (APP) are present

163 PP and ApoEr2 and more C-terminal fragments (CTF) of these proteins.

164 the alpha and beta C-terminal APP fragments (CTFs), and in the steady-state Abeta levels in the brain

165 P-processing products, C-terminal fragments (CTFs) and amyloid-beta (Abeta).

166 We report that APP C-terminal fragments (CTFs) and gamma-secretase reside in Lubrol WX detergent-

167 esion proteins and the C-terminal fragments (CTFs) are typical G-protein-coupled receptors (GPCRs) wi

168 entially amyloidogenic C-terminal fragments (CTFs) as compared with cells expressing the functional e

169 recursor protein (APP) C-terminal fragments (CTFs) by gamma-secretase underlies the pathogenesis of A

170 ced degradation of APP C-terminal fragments (CTFs) in the absence of PAFAH1B2 but not its close homol

171 id accumulation of APP C-terminal fragments (CTFs) in the synaptoneurosomes, a family of membrane-bou

172 C-terminal fragments (CTFs) of Abeta were recently shown to inhibit Abeta(1-42

173 Certain C-terminal fragments (CTFs) of Abeta42 have been shown to disrupt oligomerizat

174 viously, we found that C-terminal fragments (CTFs) of Abeta42 interfered with assembly of full-length

175 could be inhibited by C-terminal fragments (CTFs) of Abeta42.

176 e Abeta region and the C-terminal fragments (CTFs) of APP can cause transport defects.

177 r molecular mass carboxy-terminal fragments (CTFs) of APP, termed CTF-eta, in addition to the long-kn

178 reviously unidentified C-terminal fragments (CTFs) of Optic atrophy 1 (Opa1), a mitochondrial GTPase

179 Carboxyl-terminal fragments (CTFs) of TDP-43 aggregate to form the diagnostic signatu

180 contribution of TDP-43 C-terminal fragments (CTFs) to pathogenesis remains poorly understood.

181 horylated APP, of beta-C-terminal fragments (CTFs), and of beta-secretase 1 (BACE1) were also reduced

182 t NEP cleaved NPY into C-terminal fragments (CTFs), whereas silencing NEP reduced NPY processing.

183 ly cleaved to generate C-terminal fragments (CTFs).

184 ficking of APP and its C-terminal fragments (CTFs).

185 rescent, covalent triazine-based frameworks (CTFs) are obtained in an unprecedentedly mild reaction,

186 Covalent triazine frameworks (CTFs) are normally synthesized by ionothermal methods.

187 nylene-based conjugated triazine frameworks (CTFs) for efficient CO2 capture.

188 ly crystalline covalent triazine frameworks (CTFs) with ultrastrong covalent bonds (aromatic C N) fro

189 Pc1(deN)) in which NTF becomes detached from CTF.

190 f APP cleavage, and segregation of NTFs from CTFs.

191 D models for the contrast transfer function (CTF) that describe the transfer of information in the im

192 The generated CTF map highlighted distinct distributions and different

193 However, CTFs rapidly aggregated into stable cytoplasmic inclusio

194 , most of which were shown to be elevated in CTF.

195 background and allowed the visualization in CTF of proteins, such as VEGF, that were not detected wi

196 Indeed, CTF expression promotes p53-ERK interaction, which is di

197 cleavage alone is not sufficient to initiate CTF aggregation.

198 KCNE-CTFs were then further processed by PS/gamma-secretase t

199 Endogenous KCNE1- and KCNE2-CTF levels increased by 2- to 4-fold on PS/gamma-secreta

200 down prevented the generation of the 120 kDa CTF and resulted in an increase in LDL uptake into cells

201 The 120 kDa CTF was detected in the livers from humans and mice expr

202 The CSF level of this 25-kDa CTF is higher in subjects with autosomal dominant AD lin

203 ermed CTF-eta, in addition to the long-known CTF-alpha and CTF-beta fragments generated by the alpha-

204 ase activity by TAPI-1 treatment blocked LAR-CTF accumulation, demonstrating that prior ectodomain sh

205 ted in elevated LAR C-terminal fragment (LAR-CTF) levels in stably LAR-overexpressing Chinese hamster

206 Furthermore, LAR-CTF levels increased in cells lacking functional PS, ind

207 s overexpressing full-length (FL) LAR or LAR-CTFs.

208 Longer CTFs were soluble at approximately 1-80 microM, and most

209 mapping software to estimate CTFs and to map CTF fields.

210 ted, RNA was depleted, or natively misfolded CTFs were introduced into these cells.

211 Moreover, the amidated NPY CTFs protected human neuronal cultures from the neurotox

212 study supports the possibility that the NPY CTFs generated during NEP-mediated proteolysis might exe

213 Infusion of these NPY CTFs into the brains of APP (amyloid precursor protein)

214 umulation of Nrxn C-terminal fragments (Nrxn-CTF) generated by ectodomain shedding.

215 The sole expression of Nrxn-CTF decreases presynaptic release and calcium flux, reca

216 es the activity-dependent generation of Nrxn-CTF, which accumulate at presynaptic terminals lacking P

217 s of this cleavage and of any subsequent NTF-CTF interactions remain to be identified.

218 d of its N- and C-terminal fragments (PS-NTF/CTF), a mature glycosylated form of nicastrin (NCT), Aph

219 ified proteins strongly suggests that PS-NTF/CTF, mNCT, Aph-1, and Pen-2 are the components of active

220 1 activity results in robust accumulation of CTF-eta and Aeta-alpha.

221 4 suppresses transcriptional coactivation of CTF by YAP in a dose-dependent manner.

222 questions, we investigated the dependence of CTF aqueous solubility, aggregation kinetics, and morpho

223 We also applied a pyrolyzed form of CTF-HUST-4 as an anode material in a sodium-ion battery

224 Our data support a "two-hit" mechanism of CTF aggregation dependent on TDP-43 cleavage.

225 The regulation of CTF nuclear translocation and the mechanism of its apopt

226 The linear relationship of CTF-deformations was then applied in a bespoke CTF mappi

227 The sample of CTF-HUST-HC1 with abundant exposed {001} crystal facets

228 without altering the random distribution of CTFs.

229 nct distributions and different magnitude of CTFs were revealed for polarized and non-polarized kerat

230 mer formation in the absence and presence of CTFs or Abeta(21-30) and identified structural elements

231 essibility of Abeta(1-42) in the presence of CTFs was comparable to the solvent accessibility of Abet

232 the LC based CTF transducer, a wide range of CTFs was determined (10-120nN).

233 tion approach, which allows the synthesis of CTFs under mild conditions from a wide array of building

234 pment and practical large-scale synthesis of CTFs.

235 hydrophobic regions of Abeta(1-42), but only CTFs were found to bind the Abeta(1-42) region A2-F4.

236 Consequently, only CTFs but not Abeta(21-30) reduced the solvent accessibil

237 Expression of Opa1 CTFs in the intermembrane space has no effect on mitocho

238 OPN-CTF also possessed substantial pro-chemotactic activity,

239 OPN-FL and OPN-CTF did not directly bind to the CD44 standard form or C

240 release from the intact protein, because OPN-CTF was substantially more active than OPNRAA-FLR168A co

241 agment (OPN-L), and C-terminal fragment (OPN-CTF) did not have intrinsic chemotactic activity, but al

242 ctivity is compensated by the release of OPN-CTF, which assumes a new conformation and possesses subs

243 ctive than OPNRAA-FLR168A containing the OPN-CTF sequence within the intact protein.

244 rofiles (termed channel tuning functions, or CTFs) that tracked the orientation of the memorandum dur

245 charge transfer, the obtained highly ordered CTF-HUST-HC1 has superior performance in the photocataly

246 t signal was fused to the N terminus of p115 CTF accumulated in the cytoplasm and surprisingly, its e

247 tethering function of the Golgi protein p115 CTF which promotes p53-ERK interaction for the amplifica

248 precipitation studies indicate that the p115 CTF can bind to both p53 and ERK1.

249 Nuclear localization of the p115 CTF induces apoptosis.

250 demonstrate that nuclear import of the p115 CTF is required for it to stimulate the apoptotic respon

251 e, UBC9, resulted in SUMOylation of the p115 CTF.

252 In particular, CTF-HUSTs are found to be promising photocatalysts for s

253 ly occurring C-terminal fragment of PC1 (PC1-CTF) promoted Jade-1 ubiquitination and degradation, sug

254 ontrolling Jade-1 abundance, PC1 and the PC1-CTF differentially regulate Jade-1-mediated transcriptio

255 ratio, to assay RTF and individually pooled CTF and OTF samples for 80 chemokines, growth factors, c

256 s N- and C-terminal fragments (PS-NTF and PS-CTF, respectively), a highly glycosylated, mature form o

257 en the C-terminal fragment of presenilin (PS-CTF), the central component of the gamma-secretase compl

258 two minor inactive complexes (mNCT-Aph1-PS1-CTF and PS1-NTF-PS1-CTF), and (3) Pen-2 can also associa

259 complexes (mNCT-Aph1-PS1-CTF and PS1-NTF-PS1-CTF), and (3) Pen-2 can also associate with the PS holop

260 d cylindrical column of terminal fields (PV1-CTF) was identified ventrolateral to the aqueduct on the

261 lly, the longitudinal orientation of the PV1-CTF accords with that of the likewise longitudinally ori

262 e rostral and the caudal portions of the PV1-CTF consist of axonal endings, which stem from neurons s

263 The PV1-CTF is particularly dense in the rostral portion, which

264 We applied TF-OCM to quantify CTFs exerted by isolated NIH-3T3 fibroblasts embedded in

265 TFM) is a family of methods used to quantify CTFs in a variety of settings.

266 nterference screen using APP-CTF [99-residue CTF (C99)]- and Notch-specific gamma-secretase interacti

267 store or drop the memorandum, the resulting CTF was sustained in the "store" condition and rapidly e

268 Here we study the structures of selected CTFs [Abeta(x-42); x=29-31, 39] using replica exchange m

269 r acetylated tubulin, whereas the Myc-tagged CTFs are detected on randomly distributed vesicle-like s

270 oxy-terminal fragments (CTFs) of APP, termed CTF-eta, in addition to the long-known CTF-alpha and CTF

271 h five Pkd1 mouse models, we discovered that CTF plays a crucial role in Pc1(deN) trafficking.

272 We found that CTFs up to 8 residues long were soluble at concentration

273 The CTF is also able to form dimers and its dimerization is

274 els of the alternative CTF decreased and the CTF ratio was restored back to APPwt levels.

275 ross the endosomal membrane as an assay, the CTF complex activity was 650-800-fold purified from huma

276 osis; deletion of these 26 residues from the CTF diminished its proapoptotic activity.

277 emonstrate that nuclear translocation of the CTF is regulated by SUMOylation.

278 Expression of the CTF led to the phosphorylation and stabilization of p53

279 ncreased in the APP-S675E cells, whereas the CTF form that was most abundant in cells expressing APPw

280 and sufficient for axon sorting, whereas the CTF promotes wrapping through cAMP elevation.

281 The CTFs are potential candidates for separations, photocata

282 The CTFs synthesized were also readily scaled up to gram qua

283 The CTFs, but not Abeta(21-30), decreased the beta-strand pr

284 The possible role played by the CTFs in disrupting oligomerization is discussed.

285 solvent in determining the structure of the CTFs is further highlighted in ion mobility mass spectro

286 C, Hooke's equation was used to quantify the CTFs by associating Young's modulus of LC to the cell in

287 ulations in explicit solvent reveal that the CTFs adopt a metastable beta-structure: beta-hairpin for

288 in Lubrol WX-soluble membranes, wherein the CTFs derived from APP, Notch1, DCC, and N-cadherin also

289 Because these CTFs are highly hydrophobic, we asked if they themselves

290 Interestingly, these CTFs display a layered structure.

291 is, but the biological significance of these CTFs and how they are generated remain enigmatic.

292 Using an in vitro assay, we show that these CTFs indeed originate from the cleavage of Opa1 at two e

293 Thus, the accumulated TREM2 CTF thereby might limit the interaction of DAP12 with th

294 inhibition resulted in accumulation of TREM2 CTF at the plasma membrane that also interacts with the

295 agments and provokes signal transduction via CTF.

296 sphorylated TDP-43 were rapidly cleared when CTF expression was suppressed in aged Tg mice, which ame

297 To decipher the mechanism(s) by which CTFs affect Abeta42 assembly and neurotoxicity, here, we

298 with CTF solubility and the degree to which CTFs formed amyloid fibrils themselves but did not corre

299 beta42 paranucleus formation correlated with CTF solubility and the degree to which CTFs formed amylo

300 t three stages of embryonic development with CTFs cultured in collagen- or fibrin-based tissue engine