ライフサイエンスコーパス: neuraminidase

1 indlimb ischemia +/- the alpha-sialidase NA (neuraminidase).

2 za hemagglutinins), and tetramers (influenza neuraminidases).

3 coproteins, which are removed by sialidases (neuraminidases).

4 kinetics of antiviral drugs to the influenza neuraminidase.

5 le threading until they are removed by viral neuraminidase.

6 lent inhibitory effects on hemagglutinin and neuraminidase.

7 a the synergistic contributions of the viral neuraminidase.

8 f an alpha1-2-fucosidase and an alpha2-3,6,8-neuraminidase.

9 jugates were resistant to hydrolysis by H1N1 neuraminidase.

10 vercome by pretreating cells--or virus--with neuraminidase.

11 nd binding on the influenza membrane protein neuraminidase.

12 of human antibody structures with influenza neuraminidase.

13 urface viral glycoproteins hemagglutinin and neuraminidase.

14 enzymatic activity of sialyltransferases and neuraminidases.

15 o multiple different influenza A and B virus neuraminidases.

16 beta-Gal and neuraminidase 1 (NEU1) form a multienzyme complex in lys

17 Endogenous glycosidases, including neuraminidase 1 (Neu1), neuraminidase 3 (Neu3), beta-gal

18 We show increased neuraminidase 1 activity early during the progression of

19 +/-) mice have significantly decreased renal neuraminidase 1 and lactosylceramide levels.

20 have reduced activation and IL-4 production, neuraminidase 1 expression, and the levels of the glycos

21 d/or activity of LacCer synthase (GalT5) and neuraminidase 1, enzymes that mediate glycosphingolipid

22 ity Leu91Arg and Gly328Ser on N-acetyl-alpha-neuraminidase - 1 (NEU1) gene, underwent an opthalmologi

23 c-independent platelet activation, sialidase neuraminidase-1 translocation and desialylation.

24 cosidases, including neuraminidase 1 (Neu1), neuraminidase 3 (Neu3), beta-galactosidase 1 (Glb1), and

25 In neuraminidase 3 and 4 double-knockout mice, GM3 ganglios

26 Furthermore, neuraminidase 3 deficiency drastically increased storage

27 red with control, mice lacking the sialidase neuraminidase 3 have reduced HFD-induced adipose tissue

28 osaccharides by the glycosyl hydrolase human neuraminidase 3 served to validate the reliability of ki

29 ng the expression of Neu3, the gene encoding neuraminidase 3.

30 ults provide the first in vivo evidence that neuraminidases 3 and 4 have important roles in CNS funct

31 Neuraminidases 3 and 4 regulate neuronal function by cat

32 We demonstrate that 2 mammalian enzymes, neuraminidases 3 and 4, play important roles in cataboli

33 We demonstrate that pneumococcal neuraminidase A (NanA), which cleaves terminal sialic ac

34 Both hemagglutinin and neuraminidase activities of viruses bearing the TS09-C H

35 Fusion, hemadsorption, and neuraminidase activities were demonstrated for batMuV, a

36 Hemadsorption and neuraminidase activity analysis confirms the limited cap

37 are broadly protective in vivo, and inhibit neuraminidase activity by directly binding to the active

38 alk-reactive antibodies, i.e., inhibition of neuraminidase activity by steric hindrance, blocking acc

39 Interestingly, neuraminidase activity differed among virions.

40 pid and accurate quantification of influenza neuraminidase activity is achieved utilizing ultra-high

41 id provides precise measurement of influenza neuraminidase activity over a range of substrates.

42 c acids and exhibited comparable or elevated neuraminidase activity relative to human H1N1, H2N2, and

43 Current methods to investigate neuraminidase activity use small derivatized sugars that

44 hat the MPSR influences receptor binding and neuraminidase activity via an indirect mechanism.

45 he MPSR of HN modulates receptor binding and neuraminidase activity without a corresponding regulatio

46 t increase in fusion and cell killing, lower neuraminidase activity, and reduced viral growth.

47 chanism of protection by inducing endogenous neuraminidase activity, which accelerated the molecular

48 fusion, reduced receptor binding, and lower neuraminidase activity, which together result in increas

49 ion, whereas HN retains receptor binding and neuraminidase activity.

50 atMuV glycoproteins were shown to have lower neuraminidase activity.

51 vertheless, specific digestion with alpha2-3 neuraminidase (alpha2-3Neu-VWF) was sufficient to cause

52 Neuraminidase also contributes to virus binding to the s

53 A prototype design responds to viral neuraminidase, an indicator of influenza infection, and

54 Glycans are present on neuraminidase and are generally considered to inhibit an

55 and performance of the exoglycosidase enzyme neuraminidase and are used to create a fixed zone of enz

56 rmation about epitopes on influenza virus N9 neuraminidase and characterize breadth, potency, mechani

57 The phenotypic differences in the neuraminidase and fusion activity between the glycoprote

58 ation inhibition, full-length hemagglutinin, neuraminidase and hemagglutinin stalk-specific antibodie

59 Mutations in the neuraminidase and M2 genes that confer resistance to ose

60 In particular, its neuraminidase and matrix segments were derived from the

61 sialyllactose), linkage-specific sialidases (neuraminidase and sialidase S), lectins (Maakia amurensi

62 gglutinin, enhancing enzymatic activities of neuraminidase, and facilitate virus infection.

63 and has three activities: receptor binding, neuraminidase, and fusion activation.

64 or array device for the fluorogenic assay of neuraminidase, and incubated for minutes.

65 able of covering much of the surface area of neuraminidase, and the ligand binding inhibition is deri

66 iral surface glycoproteins hemagglutinin and neuraminidase, and these responses can be broadly protec

67 cognition of an erythrocyte receptor that is neuraminidase- and chymotrypsin-resistant but trypsin-se

68 Further, a broadly neutralizing anti-neuraminidase (anti-NA) mAb also required FcgammaRs to p

69 Interestingly, anti-neuraminidase antibodies weakly induced antibody-depende

70 Neuraminidase antibody levels >=80 were associated with

71 Electron microscopic analysis of two neuraminidase-antibody complexes shows that the conserve

72 fically those in the hemagglutinin stalk and neuraminidase, are currently being developed(3).

73 nin deletion variants and antigenic drift of neuraminidase, are factors that contributed to successfu

74 These results support neuraminidase as a potential target of next-generation i

75 Increasing evidence highlights neuraminidase as a potential vaccination target.

76 The findings highlight the importance of neuraminidase as a target for improved influenza virus v

77 With further optimization, this new type of neuraminidase assay may be useful in a point of care cli

78 se antibodies will inform the development of neuraminidase-based universal vaccines against influenza

79 driver of epidemic activity, indicating that neuraminidase-based vaccines and cross-reactivity assays

80 he surface glycoproteins, hemagglutinin, and neuraminidase can easily mutate their immunodominant epi

81 Influenza virus neuraminidase cleaves sialic acid groups from cell glyco

82 and H6N6 viruses, with the hemagglutinin and neuraminidase combinations being strongly lineage specif

83 wIAV genotypes and 12 distinct hemagglutinin/neuraminidase combinations with largely unknown conseque

84 robust serum antibody titers against HA and neuraminidase compared with the unadjuvanted vaccines.

85 ging signals for creating vaccines with more neuraminidase content which provide better neuraminidase

86 These neuraminidase-derived peptides, NA(181-190) (SGPDNGAVAV)

87 which increases under ischemic conditions or neuraminidase desialylation in skeletal muscle.

88 igand binding to the primary binding site of neuraminidase due to the presence of glycans.

89 removal of surface alpha2-6 sialic acids by neuraminidase, enhances gemcitabine-mediated cell death

90 omal storage disorder caused by a deficit of neuraminidase enzyme activity.

91 oving sialic acid from cell-bound IgE with a neuraminidase enzyme targeted towards the IgE receptor F

92 -antibody complexes shows that the conserved neuraminidase epitopes are located on the head of the mo

93 th influenza A virus, which also expresses a neuraminidase, exacerbates nasal colonization and diseas

94 Coinfection with neuraminidase-expressing influenza virus and S. pneumoni

95 ctose labeled with 2-aminobenzoic acid using neuraminidase from Clostridium perfringens that cleaves

96 glycans of influenza viral hemagglutinin and neuraminidase from several subtypes of influenza vaccine

97 ses may potentially be blocked by inhibiting neuraminidases, Gal-3, or MerTK.

98 onor strain by introducing hemagglutinin and neuraminidase genes derived from other strains.

99 reverse genetics with the hemagglutinin and neuraminidase genes of the eq/GA/81 wild-type (wt) virus

100 pe H1N1 holds only for the hemagglutinin and neuraminidase genes, but not for other genes.

101 f the virus, and chimeric haemagglutinin and neuraminidase genes.

102 in, but the other major surface antigen, the neuraminidase, has reemerged as a potential target for u

103 incoming viruses to cells, while the other (neuraminidase) helps release newly formed viruses from t

104 : an attachment protein called hemagglutinin-neuraminidase (HN [also called H or G depending on virus

105 of the Small Hydrophobic (SH), Hemagglutinin-Neuraminidase (HN) and Fusion (F) genes of MuVs of genot

106 t glycoprotein (G) between the hemagglutinin-neuraminidase (HN) and RNA-dependent RNA polymerase (L)

107 e functional activities of the hemagglutinin-neuraminidase (HN) and the fusion (F) proteins of the ba

108 ity to paramyxoviral RBPs with hemagglutinin-neuraminidase (HN) functionality, it presents a receptor

109 he PIV5 small hydrophobic (SH)-hemagglutinin-neuraminidase (HN) junction or deletion of PIV5 SH incre

110 one each in the fusion (F) and hemagglutinin-neuraminidase (HN) proteins.

111 the receptor-binding protein, hemagglutinin-neuraminidase (HN), and the fusion protein (F).

112 F117S (F117S), and another in hemagglutinin-neuraminidase (HN), G169R (HN169R), located in the secon

113 y the receptor binding protein hemagglutinin-neuraminidase (HN; also called H or G depending on the v

114 achment glycoprotein (G, H, or hemagglutinin-neuraminidase [HN]) and the fusion glycoprotein (F).

115 x, wherein disruption of the glycocalyx with neuraminidase increased the permeability of the cholangi

116 sin and chymotrypsin treatment sensitive but neuraminidase independent.

117 nant proteins for both the hemagglutinin and neuraminidase indicate a true avian receptor binding pre

118 Confirming the role of the GCX, neuraminidase induced the degradation of WGA-labeled GCX

119 tive effect of cellular immune responses and neuraminidase-inhibiting antibodies, additional serologi

120 ent cell-mediated cytotoxicity-mediating and neuraminidase-inhibiting functional antibodies against t

121 assay, and a newly standardized lectin-based neuraminidase inhibition (NAI) assay.

122 era for hemagglutination inhibition (HAI) or neuraminidase inhibition (NAI) titers for seroconversion

123 N8-directed antibodies displayed functional neuraminidase inhibition (NI) activity against H10N8.

124 r testing by hemagglutination inhibition and neuraminidase inhibition assays.

125 d postchallenge hemagglutination inhibition, neuraminidase inhibition, and stalk antibody titers; per

126 l antibodies that demonstrate broad binding, neuraminidase inhibition, in vitro antibody-dependent ce

127 ant from the active site while still showing neuraminidase inhibition.

128 Hemagglutination-inhibition and neuraminidase-inhibition antibody titers were determined

129 Preseason hemagglutination-inhibition and neuraminidase-inhibition antibody titers were determined

130 s involve stock- piling oseltamivir, an oral neuraminidase inhibitor (NAI), so rapidly determining th

131 , as evidenced by the finding that whereas a neuraminidase inhibitor alone did not inhibit the develo

132 lso measures susceptibility of the sample to neuraminidase inhibitor drugs.

133 influenza test followed by dispensing of the neuraminidase inhibitor oseltamivir.

134 ity and to examine antiviral efficacy of the neuraminidase inhibitor peramivir.

135 pment of IAV microplaques, the presence of a neuraminidase inhibitor together with drugs inhibiting a

136 The administration of IAP or the antiviral neuraminidase inhibitor zanamivir was therapeutic by mai

137 essed whether combinations of oseltamivir (a neuraminidase inhibitor) and T-705 (a nonspecific inhibi

138 ur outcomes were total demand for antiviral (neuraminidase inhibitor) treatment and the number of hos

139 g agents, and oseltamivir (Tamiflu), a viral neuraminidase inhibitor, disassembled the microdomains,

140 iagnosis of influenza, (2) a prescription of neuraminidase inhibitor, or (3) a rapid test positive fo

141 functional small molecule by conjugating the neuraminidase inhibitor, zanamivir, with the highly immu

142 ogenic H7N9 virus, with the exception of the neuraminidase inhibitor-resistant virus, which showed mi

143 late, and two of its variants that represent neuraminidase inhibitor-sensitive and -resistant subpopu

144 Neuraminidase inhibitors (NAIs) are the only effective t

145 Neuraminidase inhibitors (NAIs) have been widely used to

146 dence exists to support the effectiveness of neuraminidase inhibitors (NAIs) in reducing mortality wh

147 f AIVs.IMPORTANCE The chemical structures of neuraminidase inhibitors (NAIs) possess similarities, bu

148 Despite the availability of vaccines, neuraminidase inhibitors (NAIs), as the only available c

149 virus strains with reduced susceptibility to neuraminidase inhibitors (NAIs).

150 Neuraminidase inhibitors are effective for the treatment

151 hermore, the effectiveness of anti-influenza neuraminidase inhibitors has declined because of drug re

152 The available evidence on whether neuraminidase inhibitors reduce mortality in patients wi

153 Neuraminidase inhibitors showed limited effectiveness ag

154 ve been recently shown to be novel sialidase/neuraminidase inhibitors, could only be tentatively assi

155 Compared to the clinically used neuraminidase inhibitors, these two compounds showed bet

156 All isolates were sensitive to neuraminidase inhibitors.

157 er, twice-daily regimens of oral and inhaled neuraminidase inhibitors.

158 Influenza neuraminidase is an important drug target.

159 se toward the stalk domain and the conserved neuraminidase, is currently being tested in clinical tri

160 However, the function of the neuraminidase-like N11 protein is unknown because it is

161 nd targeting other viral proteins, including neuraminidase, matrix protein 2 or nucleoprotein.

162 s suggest that viruses with receptor-binding neuraminidases may occur at low levels in circulating in

163 Here, we analyse a panel of five murine anti-neuraminidase monoclonal antibodies that demonstrate bro

164 ant viruses by studying the viral fitness of neuraminidase mutants in vitro and in vivo.

165 uenza A virus (H3N2): hemagglutinin (H3) and neuraminidase (N2).

166 the influenza A virus (IAV) surface antigen neuraminidase (NA or N) showed that the conservation of

167 surface antigens hemagglutinin (HA or H) and neuraminidase (NA or N).

168 that anti-stem Abs sterically inhibit viral neuraminidase (NA) activity against large substrates, wi

169 Neuraminidase (NA) activity facilitates the release of v

170 e other two major IAV surface glycoproteins, neuraminidase (NA) and M2 ion channel, is essential for

171 le it has been shown that acquisition of the neuraminidase (NA) and matrix (M) gene segments from a E

172 The findings also establish that circulating neuraminidase (NA) and PA genes could alter the pathogen

173 had been immunized with hemagglutinin (HA), neuraminidase (NA) and the extracellular domain of matri

174 Pretreatment of RD cells with neuraminidase (NA) and trypsin greatly reduced the bindi

175 H5N1 influenza virus hemagglutinin (HA) and neuraminidase (NA) as immunogens.

176 to the HA receptor binding domain (RBD) and neuraminidase (NA) catalytic site were identified.

177 This may be attributed to a weak neuraminidase (NA) cleavage of carbon-6-linked sialic ac

178 strong HA receptor binding relative to weak neuraminidase (NA) cleavage of receptors.

179 or effects on hemagglutinin (HA) binding and neuraminidase (NA) cleavage.

180 The rescued viruses, including HA and neuraminidase (NA) double reassortants, exhibited simila

181 at HA stalk-reactive antibodies also inhibit neuraminidase (NA) enzymatic activity, prohibiting viral

182 Influenza virus neuraminidase (NA) exemplifies this concept, as it retai

183 via the oral route, but the specific role of neuraminidase (NA) for the intestinal tropism of influen

184 s reassortant (RG) viruses expressing HA and neuraminidase (NA) from 3 different H7 viruses [A/Shangh

185 Haemagglutinin (HA) and neuraminidase (NA) gene sequencing have traditionally be

186 34/2009 (Egy/09) (H5N1), with its unmodified neuraminidase (NA) gene; this virus was designated Egy/0

187 ng the wild-type (wt) hemagglutinin (HA) and neuraminidase (NA) genes from the A/blue-winged teal/Tex

188 netic analysis of the hemagglutinin (HA) and neuraminidase (NA) genes of this seal influenza A(H10N7)

189 ntaining A(H1N1)pdm09 hemagglutinin (HA) and neuraminidase (NA) genes with genetic combinations deriv

190 he hemagglutinin (HA) glycoprotein, with the neuraminidase (NA) glycoprotein being responsible for cl

191 re mutations in their hemagglutinin (HA) and neuraminidase (NA) glycoproteins that abrogate binding o

192 ntributed independently by antibody to viral neuraminidase (NA) has not been determined.

193 investigation of haemagglutinin, but whether neuraminidase (NA) has undergone antigenic change and co

194 genetic sequences of hemagglutinin (HA) and neuraminidase (NA) in an influenza A H5N2 isolate.

195 Laninamivir (LAN) is a long-acting neuraminidase (NA) inhibitor (NAI) with a similar bindin

196 Peramivir is a potent neuraminidase (NA) inhibitor for treatment of influenza

197 The therapeutic benefits of the neuraminidase (NA) inhibitor oseltamivir are dampened by

198 The neuraminidase (NA) inhibitor, oseltamivir, is a widely u

199 The neuraminidase (NA) inhibitors (NAIs) are the frontline a

200 Although neuraminidase (NA) inhibitors (NAIs) are the only class

201 Neuraminidase (NA) inhibitors (NAIs) are the only class

202 Neuraminidase (NA) inhibitors (NAIs) are the primary opt

203 ence of avian influenza viruses resistant to neuraminidase (NA) inhibitors (NAIs).

204 Currently, neuraminidase (NA) inhibitors are extensively used to tr

205 Neuraminidase (NA) inhibitors are the recommended antivi

206 ive to Food and Drug Administration-approved neuraminidase (NA) inhibitors, alternative therapies are

207 ed to introduction of the swine virus PA and neuraminidase (NA) into huH1N1.

208 Influenza virus neuraminidase (NA) is a major target for small-molecule

209 Neuraminidase (NA) is a sialidase expressed on the surfa

210 Influenza neuraminidase (NA) is a sialidase that contributes to vi

211 Neuraminidase (NA) is a sialidase that is one of the maj

212 ORTANCE Data on the immunologic responses to neuraminidase (NA) is lacking compared to what is availa

213 Neuraminidase (NA) is one of the major surface proteins

214 irus surface proteins hemagglutinin (HA) and neuraminidase (NA) is thought to be important for the tr

215 Additionally, we identified a neuraminidase (NA) mutation that allowed the virus to gr

216 The H275Y neuraminidase (NA) mutation was first detected, and an E

217 Antibodies against the neuraminidase (NA) of influenza virus correlate with res

218 0 years it has been known that antibodies to neuraminidase (NA) protect against infection during seas

219 hat antibodies targeting the influenza virus neuraminidase (NA) protein can be protective and are bro

220 The neuraminidase (NA) protein from influenza A viruses (IAV

221 nants of human humoral immune response to N9 neuraminidase (NA) proteins, which exhibit unusual featu

222 reassortant analogues containing the HA and neuraminidase (NA) segments from H1N1 2009 pandemic viru

223 emergence of pandemic hemagglutinin (HA) and neuraminidase (NA) segments in association with seasonal

224 A total of 96 hemagglutinin (HA)/neuraminidase (NA) subtype combinations were isolated, w

225 y titers to influenza hemagglutinin (HA) and neuraminidase (NA) surface antigens increase in the week

226 The neuraminidase (NA) surface glycoprotein, while diverse,

227 the growing awareness of the contribution of neuraminidase (NA) to influenza virus vaccine efficacy.

228 The H3N2 neuraminidase (NA) was of the contemporary human N2 line

229 surface glycoproteins hemagglutinin (HA) and neuraminidase (NA) with the cell surface receptor sialic

230 ed cells and recombinant hemagglutinin (HA), neuraminidase (NA), and nucleoprotein (NP) proteins.

231 (HA) (including head and stalk regions) and neuraminidase (NA), impact influenza illness and virus t

232 majority of antibodies induced by influenza neuraminidase (NA), like those against hemagglutinin (HA

233 ce membrane proteins, hemagglutinin (HA) and neuraminidase (NA), mediate protection against reinfecti

234 ubstrate to influenza viruses or its enzyme, neuraminidase (NA), releases glucose, which was detected

235 Neuraminidase (NA), the second major surface protein on

236 by antibodies against hemagglutinin (HA) and neuraminidase (NA), the two major glycoproteins on the v

237 major spike proteins, hemagglutinin (HA) and neuraminidase (NA), with the cellular receptor sialic ac

238 e neuraminidase content which provide better neuraminidase (NA)-based protection.

239 etected two mammal-adapting mutations in the neuraminidase (NA)-like protein (NA-F144C and NA-T342A,

240 re, a renewed interest in the development of neuraminidase (NA)-specific methods to characterize the

241 wo surface glycoproteins, haemagglutinin and neuraminidase (NA).

242 is revealed three mutations in HA and one in neuraminidase (NA).

243 tinin (HA) and the receptor-cleaving protein neuraminidase (NA).

244 lycoproteins, the hemagglutinin (HA) and the neuraminidase (NA).

245 particles incorporated increased numbers of neuraminidase (NA).

246 surface glycoproteins hemagglutinin (HA) and neuraminidase (NA).

247 surface glycoproteins hemagglutinin (HA) and neuraminidase (NA).

248 f viruses carrying H275Y and/or E119G in the neuraminidase (NA).

249 itical genomic segments (hemagglutinin [HA], neuraminidase [NA], and matrix [M]) of seasonal influenz

250 kdown in pneumococcal virulence, such as the neuraminidase NanA and the mannosidase SpGH92, we antici

251 ses, multisubstrate glycosidase A (MsgA) and neuraminidase (NanA).

252 unlike those organisms, S. oralis produces a neuraminidase, NanA, which cleaves terminal sialic acid.

253 The primary pneumococcal neuraminidase, NanA, which is a sialidase that catalyzes

254 Here, we show that the corresponding N9 neuraminidases (NAs) display equal enzymatic activities

255 rtant virus containing the hemagglutinin and neuraminidase of A/quail/Hong Kong/G1/1997 (H9N2) in the

256 alyses of the receptor binding hemagglutinin-neuraminidases of certain paramyxoviruses suggest that f

257 chment proteins hemagglutinin, hemagglutinin-neuraminidase, or glycoprotein (G), which are critical f

258 dues within the endothelial glycocalyx using neuraminidase perfusion decreased endothelial glycocalyx

259 entify inhibitors of Clostridium perfringens neuraminidase present in a root extract of the Pelargoni

260 The influenza virus hemagglutinin and neuraminidase proteins, expressed on the surface of VSV

261 ve for influenza A virus (H3N2), in whom the neuraminidase R292K mutation was transiently detected du

262 Unlike closely related hemagglutinin neuraminidase RBPs from other genera of the Paramyxoviri

263 Neuraminidase removal of sialic acids from wild-type neu

264 prevalence of the H275Y substitution in the neuraminidase, responsible for highly reduced sensitivit

265 rain by coadministering SA- and PSA-specific neuraminidases resulted in striking changes to the cellu

266 d PSA in cell culture studies using specific neuraminidases revealed possibly opposing roles of the t

267 Mounting evidence suggests that neuraminidase's functionality extends beyond its classic

268 An alternative neuraminidase selective for 2-3 sialic acid linkages gen

269 ng ferrets via respiratory droplets, and the neuraminidase-sensitive variant killed several of the in

270 Neuraminidase should be considered as an additional targ

271 re sialic acid neighbors the fucose, and the neuraminidase showed statistically lower action where al

272 eumococcal virulence factor, NanA, which has neuraminidase (sialidase) activity and promotes blood-br

273 2 cells and could be inhibited by Tamiflu, a neuraminidase (sialidase) inhibitor.

274 rs against influenza virus hemagglutinin and neuraminidase significantly decreased over the season am

275 pendent associations among hemagglutinin and neuraminidase subtypes.

276 d HA activities and on bacterial sialidases (neuraminidases) suggest a host-variable protective role

277 Haemagglutinin and neuraminidase surface glycoproteins of the bat influenza

278 that activated microglia release Gal-3 and a neuraminidase that desialylates microglial and PC12 surf

279 Here we characterize unusual mutant neuraminidases that have acquired the ability to bind to

280 uses have been described, none targeting the neuraminidase, the second most abundant viral glycoprote

281 electrophoresis mediated microanalysis using neuraminidase to analyze sialic acid linkages.

282 We show that the mutation that allows neuraminidase to bind cells has no apparent adverse effe

283 vity by steric hindrance, blocking access of neuraminidase to sialic acids when it abuts hemagglutini

284 ntampo showing the highest invasion rates in neuraminidase-treated erythrocytes.

285 , via FcgammaRIIB, IgG from HFD-fed mice and neuraminidase-treated IgG inhibited vascular endothelial

286 Neuraminidase-treated IgG lacking the Fc glycan terminal

287 C1galt1(-/-) neutrophils or neuraminidase-treated neutrophils failed to activate tyr

288 in the broad range of phenotypes measured by neuraminidase treatment (overall mean, 40.6% inhibition)

289 n HEL cells was greatly increased with prior neuraminidase treatment highlighting the necessity for t

290 Depletion of cell surface Sia by neuraminidase treatment inhibited MERS-CoV entry of Calu

291 Neuraminidase treatment of coated CHIR-human Ig proteins

292 Hemagglutinin and Neuraminidase undergo antigenic drift and shift, resulti

293 For Yamagata viruses, antigenic drift of neuraminidase was a major driver of epidemic activity, i

294 n our Cal/09 LAIV with PR8 hemagglutinin and neuraminidase was used to vaccinate mice, it provided en

295 development.We found that antibodies against neuraminidase were associated with significantly shorten

296 Antibodies against the N7 neuraminidase were less frequent but targeted sites clos

297 iffer by a single mutation at residue 151 in neuraminidase, which normally mediates viral exit from h

298 uenza virosomes containing hemagglutinin and neuraminidase with a PAR-2 agonist peptide (PAR-2AP) in

299 ated all-atom in silico systems of influenza neuraminidase with experimentally derived glycoprofiles

300 e inhibition of Gal-3 binding, inhibition of neuraminidase with Tamiflu, or inhibition of MerTK by UN