ライフサイエンスコーパス: neuraminidase

1 le threading until they are removed by viral neuraminidase.

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

3 3N2 strains and also inhibited mutant A/H1N1 neuraminidase.

4 get human parainfluenza type-1 hemagglutinin-neuraminidase.

5 ization of sialic acids cleaved by the viral neuraminidase.

6 nucleoprotein, and T10I in the gene encoding neuraminidase.

7 H7N9-R292K, and a structurally related H11N9 neuraminidase.

8 a the synergistic contributions of the viral neuraminidase.

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

10 jugates were resistant to hydrolysis by H1N1 neuraminidase.

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

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

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

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

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

16 echanisms through which the human sialidase, neuraminidase-1 (NEU1), promotes the interaction between

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

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

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

20 Furthermore, neuraminidase 3 deficiency drastically increased storage

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

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

23 Neuraminidases 3 and 4 regulate neuronal function by cat

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

25 activation of Neu3 sialidase, also known as Neuraminidase-3, causing conversion of GD1a and GT1b to

26 In 2004 an hemagglutinin 3 neuraminidase 8 (H3N8) equine influenza virus was transm

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

28 ted which enables the evolution of influenza neuraminidase across all subtypes (N1-N9) in human and a

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

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

31 nsmission was found to correlate with higher neuraminidase activity and a more filamentous morphology

32 ment might affect transmission, we evaluated neuraminidase activity and virion morphology of reassort

33 ed by the influenza A virus M segment impact neuraminidase activity and, perhaps through this mechani

34 We further show that neuraminidase activity in the blood can be manipulated t

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

36 segment alone resulted in an increase in the neuraminidase activity of two pairs of otherwise isogeni

37 filamentous virions, as well as reducing the neuraminidase activity of virions.

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

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

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

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

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

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

44 Concomitant with changes to neuraminidase activity, the M segment impacts the morpho

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

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

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

48 atMuV glycoproteins were shown to have lower neuraminidase activity.

49 nd NA genes that reduce viral polymerase and neuraminidase activity.

50 ficiency and can alter virion morphology and neuraminidase activity.

51 gglutinin expression, cytopathic effect, and neuraminidase activity.

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

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

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

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

56 before approximately 1907, acquired avian N1 neuraminidase and internal protein genes.

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

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

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

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

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

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

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

64 HA and neuraminidase antibody responses were assessed.

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

66 geting the viral ion-channel M2 or the viral neuraminidase are the drugs available for treatment of i

67 The glycoproteins hemagglutinin (HA) and neuraminidase are the major determinants of host range a

68 (PB1 and PA) and the viral nucleoprotein and neuraminidase, as well as 171 cellular proteins.

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

70 phenotypes were determined using the enzymes neuraminidase, chymotrypsin, and trypsin, which differen

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

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

73 neutrophils with endo-beta-galactosidase or neuraminidase converted ANCA assay results from negative

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

75 suggesting the anti-HA antibodies inhibited neuraminidase enzymatic activity through steric hindranc

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

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

78 Influenza virus neuraminidase-expressed cells, viral focus formation, an

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

80 te that specificity of both HA and the viral neuraminidase for particular sialic acid linkages determ

81 vity in the active site of influenza A viral neuraminidases for the design of novel C-6 triazole-cont

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

83 were prepared and evaluated as inhibitors of neuraminidases from four strains of influenza.

84 50 values in the low nanomolar range against neuraminidases from wild-type and oseltamivir-resistant

85 nd D354G) are necessary for maintaining full neuraminidase function in the presence of the H275Y muta

86 he inhibitory potency for both hemagglutinin-neuraminidase functions.

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

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

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

90 ed vaccines containing the hemagglutinin and neuraminidase genes of wild-type drift variant field vir

91 eed strains containing the hemagglutinin and neuraminidase genes of wild-type viruses.

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

93 Hemagglutinin-neuraminidase glycoprotein is a key protein in viral inf

94 Removal of sialic acid residues by neuraminidase had no impact on the anti-inflammatory act

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

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

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

98 -nucleotide insert between the hemagglutinin-neuraminidase (HN) and large polymerase (L) genes in a c

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

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

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

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

103 that receptor binding to their hemagglutinin-neuraminidase (HN) results in signal transmission throug

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

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

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

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

108 sin and chymotrypsin treatment sensitive but neuraminidase independent.

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

110 Neuraminidase-inhibiting antibodies were induced in >/=9

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

112 tes of hemagglutination inhibition (HAI) and neuraminidase inhibition (NAI) titer decline in the abse

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

114 frequency, led to measurable changes in the neuraminidase inhibition assay.

115 r testing by hemagglutination inhibition and neuraminidase inhibition assays.

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

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

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

119 The impact of neuraminidase inhibitor (NAI) treatment on clinical outc

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

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

122 21 patients who did not receive a concurrent neuraminidase inhibitor as part of the SOC.

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

124 assessed the efficacy of treatment with the neuraminidase inhibitor oseltamivir to reduce patient il

125 nfluenza virus-infected mice compared to the neuraminidase inhibitor oseltamivir when treatment is st

126 nfluenza virus-infected mice compared to the neuraminidase inhibitor oseltamivir when treatment is st

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

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

129 Intravenous zanamivir is a neuraminidase inhibitor suitable for treatment of hospit

130 t antiviral therapies include oseltamivir, a neuraminidase inhibitor that prevents the release of nas

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

132 Compared with no treatment, neuraminidase inhibitor treatment (irrespective of timin

133 ipant data to assess the association between neuraminidase inhibitor treatment and mortality (primary

134 We advocate early instigation of neuraminidase inhibitor treatment in adults admitted to

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

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

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

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

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

140 compare efficacy with the current frontline neuraminidase inhibitor, oseltamivir.

141 everal family clusters, and the emergence of neuraminidase inhibitor-resistant variants that show no

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) have been widely used to

145 y and uncertainty about the effectiveness of neuraminidase inhibitors (NAIs) in humans infected with

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

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

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

149 fections have been successfully treated with neuraminidase inhibitors (oseltamivir or zanamivir); how

150 All viruses were susceptible to neuraminidase inhibitors and adamantanes.

151 o investigate the association between use of neuraminidase inhibitors and mortality in patients admit

152 f including the N-hydroxyguanidine moiety in neuraminidase inhibitors are also discussed.

153 Neuraminidase inhibitors are effective for the treatment

154 d the presentation of evidence on the use of neuraminidase inhibitors as favorable or not favorable.

155 at the treatment of influenza infection with neuraminidase inhibitors decreases progression to more s

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

157 may be more likely to present evidence about neuraminidase inhibitors in a favorable manner and recom

158 Reviews that examined the use of neuraminidase inhibitors in the prophylaxis or treatment

159 Neuraminidase inhibitors showed limited effectiveness ag

160 rying markers of decreased susceptibility to neuraminidase inhibitors was reported.

161 Neuraminidase inhibitors were widely used during the 200

162 s and are also able to develop resistance to neuraminidase inhibitors without a loss in fitness.

163 Few data exist for the efficacy of neuraminidase inhibitors, which are the only readily ava

164 Viral neuraminidase inhibitors, which inhibit viral release fr

165 All isolates were sensitive to neuraminidase inhibitors.

166 Importantly, deglycosylation treatment with neuraminidase inhibits native T-currents in nociceptors

167 They show that H7N9 neuraminidase is structurally homologous to H11N9, bindi

168 cyte survival, as stripping sialic acid with neuraminidase leads to the binding of natural IgM and co

169 Partial digestion of the glycocalyx with neuraminidase led to the observation of faster peaks, as

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

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

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

173 nt H1N1 influenza viruses carrying the H275Y neuraminidase mutation predominated worldwide during the

174 of these isolates acquired hemagglutinin or neuraminidase mutations that increased virus binding to

175 Intratracheal instillation of neuraminidase (NA) 30 min prior to intratracheal adminis

176 HN stalk do not disrupt receptor binding or neuraminidase (NA) activity but are potent inhibitors of

177 Neuraminidase (NA) activity facilitates the release of v

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

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

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

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

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

183 Serum anti-HA and anti-neuraminidase (NA) antibody titers to 2009(H1N1) pandemi

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

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

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

187 B viruses with a novel I221L substitution in neuraminidase (NA) conferring high-level resistance to o

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

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

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

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

192 on in guinea pigs while selectively reducing neuraminidase (NA) gene segment packaging into virions.

193 uses that possess the hemagglutinin (HA) and neuraminidase (NA) gene segments from the newly emerged

194 34/2009 (Egy/09) (H5N1), with its unmodified neuraminidase (NA) gene; this virus was designated Egy/0

195 nes (pLAIVs) with the hemagglutinin (HA) and neuraminidase (NA) genes derived from animal influenza v

196 ccine candidates with hemagglutinin (HA) and neuraminidase (NA) genes derived from the wild-type A/Ja

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

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

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

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

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

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

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

204 Treatment of infected patients with the neuraminidase (NA) inhibitor oseltamivir was associated

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

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

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

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

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

210 a single class of available antivirals, the neuraminidase (NA) inhibitors (NAIs), is a public health

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

212 Neuraminidase (NA) inhibitors are the recommended antivi

213 Here, the development of neuraminidase (NA) inhibitors that were designed to over

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

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

216 n (HA) is the receptor-binding protein while neuraminidase (NA) is a receptor-cleaving protein that a

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

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

219 The influenza virus neuraminidase (NA) is essential for the virus life cycle

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

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

222 irus surface proteins hemagglutinin (HA) and neuraminidase (NA) is thought to be important for transm

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

224 that addition of the hemagglutinin (HA) and neuraminidase (NA) of CIV to the 2009 human pandemic vir

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

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

227 attack mechanism and that the virus uses its neuraminidase (NA) protein to prevent the recognition of

228 against viral surface hemagglutinin (HA) and neuraminidase (NA) provide sterile immunity to infection

229 the surface proteins hemagglutinin (HA) and neuraminidase (NA) requiring vaccines to be frequently u

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

231 netic analysis of the hemagglutinin (HA) and neuraminidase (NA) sequences of influenza B viruses isol

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

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

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

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

236 odies to A(H1N1)pdm09 hemagglutinin (HA) and neuraminidase (NA) were detected in IVIG preparations pr

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

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

239 d on recruitment of plasminogen by the viral neuraminidase (NA), as well as a Ser-Tyr substitution at

240 protein (NP) but not the hemagglutinin (HA), neuraminidase (NA), or M2 gene to WSN-AichiM1 abrogated

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

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

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

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

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

246 (out) TMDs from the type II membrane protein neuraminidase (NA).

247 the surface antigens, hemagglutinin (HA) and neuraminidase (NA).

248 particles incorporated increased numbers of neuraminidase (NA).

249 strated that ectodomain residue Asp286 in N2 neuraminidase (NA; Asp268 in N1 NA) present in budding-c

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

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 inally, we showed that the hemagglutinin and neuraminidase of CIV act as virulence factors.

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

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

259 , human-origin hemagglutinin (H1 and H3) and neuraminidase (particularly N2) segments were detected i

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

261 Here we reconstruct H1N1 neuraminidase phylogeny during 1999-2009, estimate the t

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

263 the human parainfluenza type-1 hemagglutinin-neuraminidase protein.

264 ng two genes encoding the haemagglutinin and neuraminidase proteins of a prototypic influenza A virus

265 ction of antibodies to hemagglutinin (HA) or neuraminidase proteins was evaluated.

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

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

268 s by coordinated action of the hemagglutinin-neuraminidase receptor-binding protein (HN) and the fusi

269 selectin ligands on leukemic progenitors by neuraminidase reduced engraftment.

270 Neuraminidase removal of sialic acids from wild-type neu

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

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

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

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

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

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

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

278 2 cells and could be inhibited by Tamiflu, a neuraminidase (sialidase) inhibitor.

279 Neuraminidases (sialidases) catalyze the removal of sial

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

281 Of the 12 neuraminidase substitutions that occurred during 1999-20

282 Although several neuraminidase substitutions were found to be necessary t

283 Herein, a putative neuraminidase (TDE0471) was identified in Treponema dent

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

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

286 RNA segments not encoding haemagglutinin and neuraminidase) that support high yield in cell culture.

287 mococcal virulence factors (such as CbpA and neuraminidases) that are not shared with other unencapsu

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

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

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

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

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

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

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

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

296 Neuraminidase treatment of coated CHIR-human Ig proteins

297 r antibody-mediated evasion in hemagglutinin-neuraminidase was found.

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

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

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