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 l studies, and evidence for an alpha-helical multimer.

3 c equilibrium between monomers and tetramers/multimers.

4 differently sized and structurally distinct multimers.

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

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

7 latelets on ultralarge von Willebrand factor multimers.

8 embly of Orai1 dimers into calcium-selective multimers.

9 mers, the smallest repeating subunits of VWF multimers.

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

11 for the detection of soluble alpha-synuclein multimers.

12 eins and consequent immune activation to RLR multimers.

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

14 ithout promoting the formation of dimers and multimers.

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

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

17 5R and L475DfsX2 p55 form aberrant reducible multimers.

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

19 the formation of disulfide-linked dimers and multimers.

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

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

22 oinhibitory role of the A2 domain within VWF multimers.

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

24 erization, and functional differences of the multimers.

25 s of protein-protein complexes and symmetric multimers.

26 he only two mammalian Igs capable of forming multimers.

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

28 resulting translation products into protein multimers.

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

30 protein may involve both monomers and small multimers.

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

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

33 SR) subdomain of triads where it forms large multimers.

34 entral dimerization domain, breaking up H-NS multimers.

35 rates mRNAs that encode head-to-tail protein multimers.

36 itopes are detected using peptide-MHC (pMHC) multimers.

37 duce the formation of detergent-soluble VDAC multimers.

38 lphaS KTKEGV repeat motifs that abrogate the multimers.

39 tion of tethered von Willebrand factor (VWF) multimers.

40 on disrupts the functional assembly of Orai1 multimers.

41 ly diverged alleles preferentially form homo-multimers.

42 reducing disulfide bonds in circulating VWF multimers.

43 and sequestered when SMN forms higher-order multimers.

44 hances overall sialic acid content of the Fc multimers.

45 ible formation of high-affinity binding BabA multimers.

46 ombosis involves von Willebrand Factor (VWF) multimers.

47 dimeric and higher order oligomeric receptor multimers.

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

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

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

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

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

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

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

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

56 Multimers, adducts, multiply charged ions, and fragments

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

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

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

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

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

62 etailed knowledge is available about how any multimer and its functions arose during evolution.

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

64 y developed peptide-exchangeable peptide/HLA multimers and artificial antigen-presenting cells for 25

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

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

67 vWF multimers and degradation fragments were quantified with

68 ted the existence of native alphaS tetramers/multimers and described engineered mutations of the alph

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

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

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

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

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

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

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

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

77 ion between ultralarge von Willebrand factor multimers and platelets.

78 ts interaction between von Willebrand factor multimers and platelets.

79 They also assemble into multimers and propagate into the infectious scrapie form

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

81 HMW multimers and the closure time with adenosine diphosphat

82 y the disulfide-bonding pattern in ficolin-3 multimers and the disulfide bonds targeted by ERp57 and

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

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

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

86 f the infectious complexes for resolution of multimers, and a thiol-containing version promoted cryst

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

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

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

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

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

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

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

94 versible Streptamers, or dye-conjugated pMHC multimers are distinct pMHC reagents tailored for T cell

95 Our results indicate that polcalcin multimers are required to stimulate high levels of effec

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

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

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

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

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

101 emonstrated ultralarge von Willebrand factor multimers at presentation.

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

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

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

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

106 substitutions accumulate that are neutral in multimers but deleterious in monomers; purifying selecti

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

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

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

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

111 3D domain-swapping proteins form multimers by unfolding and then sharing of secondary str

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

113 These multimers can be formed at physiologically-relevant conc

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

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

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

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

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

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

120 verlooked when using subtype-mismatched pMHC multimer collections.

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

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

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

124 31%, and decreased high-molecular-weight VWF multimers consistent with acquired von Willebrand syndro

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

126 s fluorescence distributions along unraveled multimer contours, and large variations in extensional r

127 An alternative explanation is that multimers could become entrenched if substitutions accum

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 ained inside the nuclear pore and undergo CA-multimer dependent CPSF6 clustering adjacent to the nucl

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

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

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

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 e efficiency of trans-splicing and extent of multimer expression decreasing as cDNA length increased.

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

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

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

145 ad54 monomers and might therefore facilitate multimer formation around DNA and 2) phosphorylation of

146 affect the amount of SSBP1 protein and alter multimer formation, but not the binding to ssDNA.

147 that disease pathology is due to defects in multimer formation.

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 a valuable tool for immunological

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

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

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

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

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

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

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

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

161 tment domain (CARD) to form filamentous homo-multimers in vitro, and this assembly mediates foci form

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

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

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

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

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

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

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

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

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

171 ically in a length-dependent manner and that multimers induce highly dynamic interactions with RNA, g

172 780CP/Cl-24 cells transfected with wt p53 or multimer-inhibiting p53(L344P) mutant, and further suppo

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

174 porating a betaA strand and displayed unique multimer interactions, including the incorporation of a

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

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

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

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

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

180 extensive multimerization in large ficolin-3 multimers leads to a high affinity for ligands and stron

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

182 ies are essential for the generation of pMHC-multimer libraries used to probe diverse, polyclonal TCR

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

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

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

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

187 SCD inhibition restores the E46K alphaS multimer:monomer ratio in human neurons, and it actually

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

189 In a database of hundreds of families of multimers, most show signatures of long-term hydrophobic

190 een explicitly observed in A1 domains of VWF multimers native to blood plasma.

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

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

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

194 or in humans, circulates as disulfide-linked multimers of a monomer.

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

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

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

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

199 Using multimers of peptide major histocompatibility complex mo

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

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

202 bly due to the loss of high-molecular-weight multimers of von Willebrand factor (VWF).

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

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

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

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

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

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

209 which bound to human telomeric G-quadruplex multimers over monomeric G-quadruplexes with high select

210 Multimer-PAGE provides a simple inexpensive biochemical

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

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

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

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

215 e lysates resembled those observed following multimer-PAGE.

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

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

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

219 Single multimer-positive T cells are sorted for the identificat

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

221 ted normally by human VWF D4 and cleaved VWF multimers, preferentially under fluid shear stress.

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

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

224 tionship between von Willebrand factor (VWF) multimer profile and heart valve diseases (HVD).

225 Not only does the analysis of the VWF multimer profile provide an excellent evaluation of HVD

226 into a heterogeneous collection of misfolded multimers, ranging from soluble oligomers to insoluble a

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

228 fast and standardized generation of any pMHC multimer reagent from a single precursor ("FLEXamer").

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

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

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

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

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

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

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

236 Results: Despite the multimers showing higher alphavbeta6 integrin affinities

237 Despite the multimers showing higher alphavbeta6 integrin affinities

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

239 forms higher order complexes and that these multimers signal.

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

241 large ficolin-3 multimers, thereby reducing multimer size and ligand-binding affinity.

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

243 isulfide bonds in ficolin-3 and reducing its multimer size.

244 tigated by interventions known to reduce VWF multimer size.

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

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

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

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

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

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

251 ments to highly symmetric or pseudosymmetric multimer structures.

252 Dynamics (MD) simulations of non-grafted vWF multimers subject to a shearing flow were used as input

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

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

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

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

257 e and disrupt the structure of the integrase multimer that is required for the HIV-1 maturation.

258 intermolecular disulfide bonds in ficolin-3 multimers that are reduced by ERp57.

259 perature affect the capacity of H-NS to form multimers that condense DNA and restrict gene expression

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

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

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

263 molecular disulfide bonds in large ficolin-3 multimers, thereby reducing multimer size and ligand-bin

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 restrained adhesion of von Willebrand factor multimers to platelets and microthrombosis, which result

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

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

272 nsion-dependent activation of individual VWF multimers under a range of ionic strengths and pH levels

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

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

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

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

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

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

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

280 Using DNA barcode-labeled MHC-I multimers, we find CD8(+) T cell populations recognizing

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

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

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

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

285 hase such that covalent head-to-tail protein multimers were translated.

286 cromolecular conformation information of vWF multimers were used for training the RFA.

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 trans-splicing, generating covalent protein multimers with novel functions within cells, and produci

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

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