ライフサイエンスコーパス: multimer

1 s but not WTS seeds or fibrils (aSyn(30-110) multimers).

2 s are individually functional within a given multimer.

3 on disrupts the functional assembly of Orai1 multimers.

4 for the detection of soluble alpha-synuclein multimers.

5 le for the degradation of mislocalized MEC-2 multimers.

6 and sequestered when SMN forms higher-order multimers.

7 ithout promoting the formation of dimers and multimers.

8 ly in alpha-helix-rich tetramers and related multimers.

9 is enriched in hyperactive "ultra-large" VWF multimers.

10 5R and L475DfsX2 p55 form aberrant reducible multimers.

11 gests the occurrence of SL-SH oleosin dimers/multimers.

12 the formation of disulfide-linked dimers and multimers.

13 lebrand factor (VWF) in smaller, less active multimers.

14 tryptophan-rich protein (SLTRiP) forms large multimers.

15 oinhibitory role of the A2 domain within VWF multimers.

16 ng to the lipid bilayer and the formation of multimers.

17 erization, and functional differences of the multimers.

18 s of protein-protein complexes and symmetric multimers.

19 he only two mammalian Igs capable of forming multimers.

20 P is not limited to an increase in large VWF multimers.

21 resulting translation products into protein multimers.

22 to form disulfide-linked dimers and to form multimers.

23 protein may involve both monomers and small multimers.

24 hances overall sialic acid content of the Fc multimers.

25 the ability of Tat to transport cross-linked multimers.

26 results in the differently 3D domain-swapped multimers.

27 ible formation of high-affinity binding BabA multimers.

28 ccurs concomitantly with a decrease in Gal80 multimers.

29 ombosis involves von Willebrand Factor (VWF) multimers.

30 latable PLM, confirming the existence of PLM multimers.

31 l resulted in self-assembling, active enzyme multimers.

32 evels (before and after stimulation) and VWF multimers.

33 d factor multimers into smaller, less active multimers.

34 e tetrameric, pentameric and hexameric N-RNA multimers.

35 dimeric and higher order oligomeric receptor multimers.

36 ly diverged alleles preferentially form homo-multimers.

37 c equilibrium between monomers and tetramers/multimers.

38 differently sized and structurally distinct multimers.

39 reducing disulfide bonds in circulating VWF multimers.

40 ar the C termini of molecules within PrP(Sc) multimers.

41 on of hyperreactive ultra-large VWF (UL-VWF) multimers.

42 latelets on ultralarge von Willebrand factor multimers.

43 embly of Orai1 dimers into calcium-selective multimers.

44 mers, the smallest repeating subunits of VWF multimers.

45 m/z-coincident species, both conformers and multimers.

46 and accumulation of low-molecular-weight vWF multimers (+40+/-5%, P<0.0001) and vWF degradation fragm

47 ant degradation of high-molecular-weight vWF multimers (-9+/-1%, P<0.0001) and accumulation of low-mo

48 ersed the strong membrane interaction of the multimer-abolishing alphaS variant but also restored mul

49 er repeat mutants in human neural cells, all multimer-abolishing but no multimer-neutral mutants caus

50 The multimer-abolishing variants became enriched in buffer-i

51 roducible methods to compare alpha-synuclein multimer abundance between complex biological samples.

52 Moreover, ultra-large VWF multimers accumulate in the plasma of fVIII(-/-) mice af

53 activity in cTTP serum, which prevented VWF multimer accumulation on endothelial cells, or by an ant

54 Additional experiments suggest that Mto1/2 multimers act to multimerize the fission yeast gamma-tub

55 Multimers, adducts, multiply charged ions, and fragments

56 down using major histocompatibility complex multimers against the immunodominant H4, H7, H13, H28, a

57 says, and staining with peptide:MHC class II multimers, all of these have significant technical const

58 lization of peptide-major histocompatibility multimers, along with imaging techniques for static mult

59 The ratio of multimer (alphaS80) to monomer (alphaS17) increased line

60 ring agent as evidenced by FCS and gel-based multimer analysis.

61 These clones bound the A2-GPC3367 multimer and secreted interferon-gamma when cultured wit

62 reduced levels of high-molecular weight VWF multimers and a corresponding prolongation of bleeding t

63 Willebrand factor (VWF) rapidly loses large multimers and binds poorly to platelets and subendotheli

64 able analyses showed that the values for HMW multimers and CT-ADP at the end of TAVR were each associ

65 is characterized by the absence of large VWF multimers and decreased platelet-binding function.

66 vWF multimers and degradation fragments were quantified with

67 nificantly reduced vWF levels but normal vWF multimers and impaired laser-induced thrombus formation,

68 the primary cause for the loss of large VWF multimers and LVAD-associated bleeding remains circumsta

69 large molecular-size entities and to smaller multimers and mixtures of species.

70 We further investigated the recovery of HMW multimers and monitored these changes with PFA-CADP in a

71 the fundamental relationship between alphaS multimers and monomers in living neurons, we performed s

72 Compared to current ASOs, these multimers and multi-targeting oligonucleotides (MTOs) pr

73 endent and included the formation of various multimers and multiple Cu(I/II) binding.

74 suggests that alpha-syn exists as metastable multimers and not solely as a natively unfolded monomer.

75 on the number of monomers in individual VWF multimers and on the self-association of individual VWF

76 ion between ultralarge von Willebrand factor multimers and platelets.

77 ed ANGPT1 p.A119S formed a reduced amount of multimers and showed reduced binding capability to its r

78 HMW multimers and the closure time with adenosine diphosphat

79 e of RAF dimers and potentially higher-order multimers and their involvement in cell signaling, and s

80 y engage in homophilic trans-interactions as multimers and they are required for diverse neurodevelop

81 ble before rVWF infusion, a reduction in VWF multimers and VWF activity was observed.

82 eding tendency that is linked to loss of vWF multimers and/or thrombocytopenia.

83 ndant spectral features (adducts, fragments, multimers) and calculation of the underlying chemical fo

84 dence suggests that hDAT might function as a multimer, and its oligomerization may be relevant to add

85 s, VWF activity (VWF:Act), antigen (VWF:Ag), multimers, and factor VIII coagulant activity were virtu

86 f 4-1BB (CD137), binding to CMV-specific HLA multimers, and interferon-gamma production.

87 uding large molecular-size entities, smaller multimers, and mixtures of assembled species.

88 In biochemical studies, CS disrupted TCR multimers, apparently by displacing cholesterol, which i

89 ized by AFM imaging, we estimate that in VWF multimers approximately one-half of the constituent dime

90 Acquired abnormalities of VWF multimers are associated with aortic and mitral prosthes

91 Fluorochrome-conjugated peptide-MHC (pMHC) multimers are commonly used in combination with flow cyt

92 chrome-conjugated peptide-MHC (pMHC) class I multimers are staple components of the immunologist's to

93 Disulfide-dependent B27 H chain dimers and multimers are stronger ligands for LILRB2 than HLA class

94 ause only GPIHBP1 monomers-and not dimers or multimers-are capable of binding LPL.

95 We find that APOBEC3G forms high-order multimers as a function of protein concentration.

96 ULVWF multimers, as are present in patients with thrombotic mi

97 full-length HIV IN provide new insight into multimer assembly and suggest additional approaches for

98 found that prior to membrane curvature, Gag multimers associate with a specific subset of UDMs conta

99 access to multiple cleavage sites of the VWF multimer at the same time.

100 emonstrated ultralarge von Willebrand factor multimers at presentation.

101 ha-syn promptly organizes into physiological multimers at synapses.

102 and providing structural information of the multimers at the same time.

103 topenic purpura (cTTP) who cannot cleave VWF multimers because of genetic ADAMTS13 deficiency, we inv

104 Better MHC-multimer binding and slower multimer release are thought

105 , large disparities were found comparing CTL multimer binding with peptide sensitivity.

106 n-specific T cells detectable by HLA-peptide multimer binding.

107 FtsA forms multimers both in vitro and in vivo, but little is known

108 in type-1 repeats 13 (ADAMTS-13) cleaves VWF multimers, but both have been associated with prognosis

109 ome maintenance role by unlinking chromosome multimers, but their mechanism of action has remained st

110 leavage of ultra-large molecular-weight rVWF multimers by ADAMTS13 (a disintegrin and metalloproteina

111 Formation of native PulD-multimers by mixing protomers that differ in N3 domain s

112 be caused by excessive cleavage of large VWF multimers by the metalloprotease ADAMTS-13 in an LVAD-dr

113 3D domain-swapping proteins form multimers by unfolding and then sharing of secondary str

114 tal evidence supports the concept that Abeta multimers can act as seeds and structurally corrupt othe

115 These multimers can be formed at physiologically-relevant conc

116 IN, which self-associates into higher-order multimers, can form a functional intasome, reconcile the

117 alpha-Synuclein multimers captured by directly cross-linking soluble lys

118 ine DI-phosphate [PFA-CADP]), reflecting HMW multimers changes, could be used to monitor in real-time

119 TRPC3 has been long suggested to form hetero-multimer channels with TRPC6 and function as diacylglyce

120 ore, our experiments indicate that alpha-syn multimers cluster synaptic vesicles and restrict their m

121 We propose a model in which alpha-syn multimers cluster synaptic vesicles, restricting their t

122 verlooked when using subtype-mismatched pMHC multimer collections.

123 g/ml and the antibody pairs recognized Abeta multimers comprised of either synthetic standards, or en

124 ular complexes forming large, densely packed multimers comprising up to several thousand monomers.

125 se distance restraints, construction of homo-multimers, consideration of small-angle X-ray scattering

126 31%, and decreased high-molecular-weight VWF multimers consistent with acquired von Willebrand syndro

127 cted using panels of color-coded peptide-HLA multimers containing epitopes predicted by a computer al

128 high-molecular-weight von Willebrand factor multimers could reduce platelet adhesion.

129 nfecting phage and in resolution of prophage multimers created by generalized recombination.

130 The presence of HMW-multimer defects and a high value for a point-of-care he

131 time course of the induction/recovery of HMW multimers defects under instantaneous changes in shear s

132 The complement regulatory function of VWF multimers depends on their size.

133 Lastly we discuss findings showing that multimers derived from LRRC8A (leucine-rich repeat conta

134 nd subsequently resulted in abundant soluble multimer detection via multimer-PAGE.

135 Dephosphorylation of the PLM multimer does not change sodium pump activity.

136 In summary, Ab stabilization of pMHC multimers during T cell staining extends the range of TC

137 ts, and purified dimers, trimers, and larger multimers elicited similar levels of cross-subtype bindi

138 Barcode-labeled pMHC multimers enable the combination of functional T-cell an

139 Smaller VWF multimers enhance cleavage of C3b but large and ultra-la

140 enzyme is a hexamer, only the second form II multimer ever solved and the first RubisCO structure obt

141 ly reconstitutes into liposomes as dimers or multimers, F45L, V209M and F220C rhodopsins behave as mo

142 We used a fluorescent Ara h 2 multimer for affinity selection of Ara h 2-specific B ce

143 exponentially decaying size distribution of multimers for recombinant VWF as well as for VWF derived

144 s of protein-protein complexes and symmetric multimers for their own analysis.

145 mbrane by fusion to a RAS CAAX motif induces multimer formation but activates RAF/MAPK only if the di

146 ement in cell signaling, and showed that RAF multimer formation can result from multiple mechanisms a

147 hat the TSP-N domain is responsible for homo-multimer formation of Nel and its heparin-binding activi

148 verlapping melting and refolding curves, G3T multimers (G3T units covalently attached to each other)

149 by peptide-major histocompatibility complex multimer-guided cell sorting.

150 nction of alphaS at vesicles, and abrogating multimers has pathogenic consequences.

151 ghly reproducible hysteretic behavior of G3T multimers has the potential to be used in the design of

152 Peptide-MHC (pMHC) multimers have become one of the most widely used tools

153 of C3b but large and ultra-large VWF (ULVWF) multimers have no effect on C3b cleavage and permit defa

154 Very large VWF multimers have the greatest thrombogenic activity, which

155 VWF and is enriched in high molecular weight multimers (HMWM).

156 the stoichiometry of soluble alpha-synuclein multimers in brain tissue lysates.

157 ent resolution to directly visualize protein multimers in cells.

158 Hagfish Vwf formed high-molecular-weight multimers in hagfish plasma and in stably transfected CH

159 osed that alphaS forms soluble alpha-helical multimers in healthy neurons.

160 ng ultra-large von Willebrand factor (ULVWF) multimers in long string-like structures that initiate p

161 hrombospondin-5 were preferentially bound by multimers in pancreatic cancer patient samples relative

162 microscopy identified monomers, dimers, and multimers in purified fibulin-4 preparations with sizes

163 arent inability of this factor to engage Rev multimers in the context of large viral Rev/RNA ribonucl

164 Arm movement gives rise to the three multimers in the crystal structures and also explains th

165 Here, we have made alphaS multimers in vitro using arachidonic acid (ARA), one of

166 s, however, suggest that it can form soluble multimers in vivo that have significant secondary struct

167 dicating the possibility that hpol eta forms multimers in vivo.

168 ial cells and stored as ultra-large (UL) VWF multimers in Weibel-Palade bodies.

169 n spiked into lacritin-depleted tears formed multimers, in keeping with approximately 0.6 muM TGM2 in

170 tion of a second mechanism through which VWF multimers incorporate into a fibrin network.

171 Consistent with these findings, pMHC-II multimers incorporating peptide flanking residue modific

172 that FliG has a significant tendency to form multimers independently of other flagellar components.

173 al assembly and calcium selectivity of Orai1 multimers independently of Stim1 levels.

174 tory potential in other cell types, EWS-FLI1 multimers induce chromatin opening and create de novo en

175 780CP/Cl-24 cells transfected with wt p53 or multimer-inhibiting p53(L344P) mutant, and further suppo

176 ibit the processing of von Willebrand factor multimers, initiating a rare and life-threatening disord

177 we postulated that NAC might cleave the VWF multimers inside occlusive thrombi, thereby leading to t

178 nd on the self-association of individual VWF multimers into larger structures.

179 a1R agonists promote dissociation of sigma1R multimers into monomers, which then interact with DAT to

180 yperactive ultra large von Willebrand factor multimers into smaller, less active multimers.

181 umulation of hyperphosphorylated soluble tau multimers into the synaptic compartment was noted in dem

182 unidentate attachments and to self-assembled multimers, involving formation of intralayer horizontal

183 suggest that the mechanism by which secretin multimers kill psp null cells is by causing a profound d

184 ptide-major histocompatibility complex (MHC) multimers labeled with individual DNA barcodes to screen

185 ither the hinge or tail piece of monomers or multimers leads to molecules with enhanced sialylation t

186 t with either subtype-matched or HLA-A*02:01 multimers loaded with 145 different melanoma-associated

187 ic cytokine staining in conjunction with HLA multimers loaded with tumor peptide and antigen-specific

188 olved mass spectra, for example, complicated multimer mass spectra and norovirus capsid mass spectra

189 hly thrombogenic von Willebrand factor (VWF) multimers may accelerate renal and cardiovascular compli

190 The use of soluble CD40L multimers may help to improve vaccination responses in H

191 over a wide range, and the multiply charged multimers (MCMs) present in the ion mobility/mass spectr

192 ng tagged r-VKORC1 revealed that VKORC1 is a multimer, most likely a dimer.

193 neural cells, all multimer-abolishing but no multimer-neutral mutants caused frank neurotoxicity akin

194 After the initial implantation, HMW multimers normalized in patients without aortic regurgit

195 Based on a regular pattern of multimers observed in analytical ultracentrifugation, an

196 demonstrated that induction/recovery of HMW multimers occurs within 5 minutes.

197 4 and beta(2)GPI conformation (or ultralarge multimer of von Willebrand factor oligomerization or fun

198 Many remodelers contain pairs or multimers of actin-related proteins (ARPs) that contact

199 evidence for the formation of alpha-helical multimers of alphaS in the presence of a biologically re

200 Acrp30 circulates as multimers of high, middle, and low molecular weight.

201 The FRET experiments indicated that the multimers of membrane-bound alpha-synuclein exhibit defi

202 avidity assessment by NTA-His tag-containing multimers of naturally occurring polyclonal T cell respo

203 clones demonstrated that staining with pMHC multimers of seven distinct subtypes of the HLA-A*02 all

204 Furthermore, larger ribbonlike DPs that were multimers of the NMJ building unit are found at synapses

205 omplicated structure containing higher-order multimers of the transposase.

206 tion/recovery of high molecular weight (HMW) multimers of von Willebrand factor defect could be insta

207 nt of defects in high-molecular-weight (HMW) multimers of von Willebrand factor or point-of-care asse

208 emand imposed by local genesis of ultralarge multimers of von Willebrand factor.

209 Loss of high-molecular-weight multimers of VWF.

210 e results suggest that pORF30 may exist as a multimer or participate in higher-order assemblies durin

211 issociated) or dissociating into lower order multimers or a number of product ions for each m/z.

212 s-linking of biotinylated HA in streptavidin multimers or supramolecular complexes with the inflammat

213 e response is determined by the abundance of multimers over dimers within a cluster population: the m

214 Multimer-PAGE provides a simple inexpensive biochemical

215 Once the multimer-PAGE technique was validated, relative stoichio

216 ) increased linearly with protein input into multimer-PAGE, suggesting to some extent, multimers were

217 Here we developed a method, termed "multimer-PAGE," that combines in-gel chemical cross-link

218 e lysates resembled those observed following multimer-PAGE.

219 d in abundant soluble multimer detection via multimer-PAGE.

220 ing tendency and VWF quantity, activity, and multimer pattern.

221 normalization of VWF/factor VIII levels and multimer pattern.

222 It is now apparent that protein multimers play an important role in RAF activation and t

223 ections, we demonstrate that dimers, and not multimers, potentiate the reassembly and reorganization

224 We conclude that normal plasma VWF multimers prevent complement activation and steer the co

225 circulating ultralarge von Willebrand factor multimers, prevented severe thrombocytopenia, and reduce

226 6) each monomer (whether it was free or in a multimer) primarily bound up to 3 Cu(I) ions, whereas at

227 d was associated with a lower normalized VWF multimer ratio than in patients without bleeding.

228 PFA-CADP profiles mimicked HMW multimers recovery both in transcatheter aortic valve im

229 omponent as it cleaves von Willebrand factor multimers, reduces platelet adhesion and aggregation, an

230 orted by in vitro data demonstrating the VWF multimer-reducing properties of NAC in solution.

231 itions 166 or 167, and are unable to bind cI multimers, regain substantial cI binding when amino acid

232 Better MHC-multimer binding and slower multimer release are thought to reflect stronger TCR-pep

233 monstrated that a proportion of these UL-VWF multimers remain anchored to the activated endothelium.

234 stoichiometry and cellular location of these multimers remain unclear because of the lack of technolo

235 oplasmic reticulum and is essential for long multimers required for hemostatic function.

236 he biosynthesis of VWF high-molecular-weight multimers requires spatial separation of each step becau

237 ating that different complexes, monomers and multimers, respectively, are responsible for these two a

238 ands into DNA- or RNA G-quadruplex mono- and multimers, respectively.

239 lacement of Cys-575 in the IgM tail piece of multimers resulted in monomers with enhanced sialic acid

240 Results: Despite the multimers showing higher alphavbeta6 integrin affinities

241 Despite the multimers showing higher alphavbeta6 integrin affinities

242 ast condensin, with the result that only the multimer shows ATP-enhanced DNA-compaction.

243 forms higher order complexes and that these multimers signal.

244 ell-free expressed mMOMP-tNLPs contain mMOMP multimers similar to the native MOMP protein.

245 Von Willebrand factor (VWF) multimer size is controlled through continuous proteolys

246 sulfide bonds in VWF, thereby decreasing VWF multimers size and hence their prothrombotic potential.

247 luenced Ag recognition as determined by CD1d multimer staining and CD1d-restricted functional respons

248 pMHC multimer staining of tumor-specific, autoimmune, or MHC

249 find that this inexpensive addition to pMHC multimer staining protocols also allows improved recover

250 Unexpectedly, tetramers/multimers still formed in cells expressing each of 14 se

251 nting missense substitutions influencing VWF multimer structure and interactions with platelet GPIbal

252 of mutant monomer incorporation in the final multimer structure of plasma VWF.

253 ments to highly symmetric or pseudosymmetric multimer structures.

254 d a reduced propensity for forming dimers or multimers, suggesting that W109 might play a more direct

255 complexes using fluorochrome-conjugated TCR multimers suggests that nonamer- and decamer-linked pept

256 tudy, using the novel NTA-His tag-containing multimer technology, we quantified the TCR:pMHC dissocia

257 these rare cells, we developed a peptide-MHC multimer technology, which uses reversible Ni(2+)-nitril

258 ated proteins, MAP2 and Tau, is stronger for multimers than for monomers.

259 and pathological mutants of alphaS form less multimers than wild-type alphaS.

260 nt with YbAnbu forming defined 12-14 subunit multimers that differ in shape from both HslV and 20S pr

261 f VWF domain A2 in peptide substrates or VWF multimers that had been sheared; native (unsheared) VWF

262 sity to localize in the nucleus and generate multimers that subsequently serve as templates for HV-de

263 ha-synuclein occurs as a monomer and several multimers, the latter of which may be important for the

264 an ordered process involving A3G dimers and multimers thereof.

265 ing from the level of monomeric subunits and multimers to closed spherical shells, and to hypothesize

266 We used A2-GPC3367 multimers to detect, select for, and clone GPC3-specific

267 We used CMV-specific HLA multimers to enumerate CMV-specific T-cell numbers and s

268 E4-ORF3 self-assembles into multimers to form a nuclear scaffold in infected cells a

269 rs as immunogens, and subsequently relies on multimers to pre-screen and magnetically enrich the resp

270 In contrast, the addition of soluble CD40L multimers to T cell/B cell cultures redirects B cell dif

271 in elevated plasma levels of ultra-large VWF multimers (ULVWF), which are prone to induce platelet ag

272 or C-terminus, were rapidly oxidized forming multimer units within thirty minutes.

273 These multimers unravel, bind platelets, and wave in the direc

274 topic labeling to facilitate HDX analysis of multimers using HIV-1 reverse transcriptase (RT) as a mo

275 e co-synthesized as homo- or heterodimers or multimers via phosphodiester linkers that are stable in

276 cation of the protonated amine along the MDA multimer was found to influence the gas phase stability

277 come occurred even though a reduction in VWF multimers was observed, demonstrating that NAC was effic

278 ual aortic regurgitation, no recovery of HMW multimers was observed.

279 the proportion of high molecular weight VWF multimers was reduced, despite severely decreased ADAMTS

280 In considering structural models of PrP(Sc) multimers, we identified an obstacle to tight packing th

281 von Willebrand factor multimers were abnormal in 1 of 26 normal aortic valve r

282 to multimer-PAGE, suggesting to some extent, multimers were also formed during electrophoresis.

283 t significantly reduced, pathological UL-VWF multimers were also observed in murine plasma following

284 hat had been sheared; native (unsheared) VWF multimers were resistant.

285 Ubiquitin multimers were used to show that after glycinylation and

286 10-residue N-terminal extension, which forms multimers when isolated from Escherichia coli.

287 We found that CyaA forms mainly multimers when refolded by dialysis, dilution, or buffer

288 ollowing tissue disruption and readily forms multimers when this lipid-protein complex is preserved.

289 oximately 8-11 the fully oxidized monomer or multimer (where all Cys formed a disulfide bond) primari

290 stabilized and then lock the spidroins into multimers, whereas CT on the other hand is destabilized

291 s in the form of disulfide-linked dimers and multimers, whereas wild-type GPIHBP1 was predominantly m

292 ainly as a large protein complex, possibly a multimer, which is not altered by SR Ca(2+) depletion.

293 d by endothelial von Willebrand factor large multimers, which can be reversed with exogenous ADAMTS13

294 , but activation also generates higher-order multimers, whose nature and function are poorly understo

295 abled development of CD1a tetramers and CD1a multimers with carbohydrate backbones (dextramers), whic

296 condary structure to domains, molecules, and multimers with each level represented in an identical da

297 yl farnesoate stimulates dissociation of Met multimers with subsequent association with SRC.

298 elf-propagating, and often fibrillar protein multimers with the capacity to seed, or template, the co

299 crease in shear stress and a recovery of HMW multimers within minutes of implantation which was susta

300 u is consistent with the presence of defined multimers, X-ray diffraction data in solution and negati