neuraminidase assay based on PNA hemagglutanation is highly sensitive, reproducible and can be used as a tool to detect sialidase activity in anaerobic bacteria, particularly, in species of the bacteroides fragilis group
subcloning of carbohydrate-binding module CBM40 of sialidase, showing high affinity for sialic acid and specificity to alpha(2,3), alpha(2,6), and alpha(2,8)-linked sialosides. Creation of polypeptides containing up to four CBM40 modules in tandem show increased affinities compared with the single module molecule. Variation in linker length has little effect on affinity
virtual screening method for inhibitors based on consensus scoring and ligand efficiency indices, which allows the combination of pharmacodynamic and pharmacokinetic properties into unique measures
construction of highly infectious laryngotracheitis virus expressing H5 hemagglutinin and/or N1 neuraminidase and use in ocular immunization of chickens. Animals immunized with laryngotracheitis virus expressing neuraminidase N1 died after subsequent H5N1 avian influenzy virus challenge, although survival times were prolonged compared to non-vaccinated controls. In contrast, all chickens vaccinated with either laryngotracheitis virus expressing hemagglutinin H5 alone, or hemagglutinin H5 and neuramindase N1 simultaneously, survived without showing any clinical signs
in fibroblasts from patients with sialidosis, oversialylated lysosomal membrane protein Lamp-1 enhances lysosomal exocytosis. Silencing of Lamp-1 reverts this phenotype by interfering with the docking of lysosomes at the plasma membrane
in macrophages from isoform Neu1 deficient mice, a model for sialidosis, oversialylated lysosomal membrane protein Lamp-1 enhances lysosomal exocytosis. Silencing of Lamp-1 reverts this phenotype by interfering with the docking of lysosomes at the plasma membrane. In Neu1-/- mice the excessive exocytosis of serine proteases in the bone niche leads to inactivation of extracellular serpins, premature degradation of VCAM-1, and loss of bone marrow retention
isoform Neu2 mRNA and enzymatic activity are significantly increased in hypertrophic myofibers. Constitutive activation of AKT or Igf-1 treatment as well as treatment with vasopressin or trichostatin results in rise in Neu2 activity. Myofiber atrophy obtained by dexamethasone treatment or starvation triggers a significant loss of Neu2 activity and is paralleled by downregulation of Neu2 transcript levels
isoform Neu3 plays a key role in skeletal muscle differentiation by strictly modulating the ganglioside content of adjacent cells, with special regard to GM3. Induced down-regulation of NEU3, even when partial, totally inhibits cell's capability to differentiate by increasing the GM3 level above a critical point, which causes epidermal growth factor receptor inhibition and ultimately its down-regulation and an higher responsiveness of myoblasts to the apoptotic stimuli
isolation of mutants from H5N1-infected patients to explain the molecular basis of resistance to oseltamivir. Mutants are resistant to oseltamivir but still strongly inhibited by zanamivir owing to an altered hydrophobic pocket in the active site of the enzyme required for oseltamivir binding
mice vaccinated with an engineered enzymatically deficient mutant trans-sialidase containing the catalytic domain without the immunodominant shed acute phase antigen repeats SAPA, are highly protected against Trypanosoma cruzi infection. Adult male BALB/c mice immunized with mutant protein are protected against challenge with a lethal dose of Trypanosoma cruzi trypomastigotes. The protected immunized mice developed no clinical or tissue evidence of infection throughout the study
neuraminidase activity is significantly higher in septic patients compared with nonseptic patients and healthy volunteers. Desialylation by increased neuramindase activity may contribute to the alternations in red blood cell rheology
study on functional compatibility of hemagglutinin and neuraminidase on the oligosaccharide level, through measuring the receptor-binding and substrate specificities of reassortant/passage human-avian variant virus pairs. Selection of the high-yield variants of the human-avian reassortants leads either to twofold decrease in the affinity of HA for most alpha2-3-sialosides and the appearance of affinity for alpha2-6-sialosides like in the H3N2 reassortant, or to decreasing the hemagglutinin affinity for Neu5Acalpha2-3Galbeta1-3GlcNAc and Neu5Acalpha2-3Galbeta1-3(Fucalpha1-4)GlcNAc in the H3N1 reassortant, or to enhancing the ability of neuraminidase to discriminate between alpha2-3/2-6 substrates in the H4N1 reassortant
study on susceptibility of Neu3 transgenic mice to induction of colonic aberrant crypt foci by azoxymethane. Injection of with azoxymethane results in decreased GM3 and increased lactosylceramide content in transgenic colon mucosa. Up-regulation of Neu3 is important to the promotion stage of colorectal carcinogenesis
the induction of hST3Gal V, which synthesizes ganglioside GM3 and reduction of Neu3 by PMA, are linked for the expression of differentiation marker protein, CD41b surface antigen. Neu3 overexpression inhibits the PMA-induced ERK1/2 and p38 MAPK phosphorylation in the K-562 cells. Down-regulation of expression of CD41b surface antigen is dependent on expression of Neu3 gene. Neu3 inhibitor 2-deoxy-2,3-didehydro-D-N-acetylneuraminic acid induces morphological changes, showing megakaryocytic differentiation of K562 cells, with expression of CD41b surface antigen, while specific glucosylceramide synthase inhibitor 1-phenyl-2-decanoylamino-3-morpholino-1-propanol inhibits megakaryocytic differentiation of K-562 cells. Molecular mechanisms involved in Neu3-involved inhibition of CD41b surface antigen expression in K-562 cells include that Neu3 degrades membrane sialic acids and the resulting signaling pathway of the PKC/ERKs/p38 MAPK is down-regulated, causing a decrease in CD41b surface antigen expression and inhibition of megakaryocytic differentiation of K562 cells
treatment of red blood cells with enzyme modifies their shape in a dose-dependent fashion. Cells become more spherical, and alterations remain for at least ten hours. Changes are similar to changes during sepsis
treatment with Clostridium perfringens neuraminidase which is highly homologous to human Neu1 decreases human smooth muscle cell proliferation, even in cultures that do not deposit elastin. Pretreatment of aortic smooth muscle cells with exogenous neuraminidase abolishes their mitogenic responses to recombinant platelet-derived growth factor PDGF-BB and insulin-like growth factor IGF-2
bacterial neuraminidases functions as the predominant neuraminidase when influenza virus neuraminidase is inhibited to promote the spread of infection and to inactivate the neutralization activity of saliva. Neuraminidase from bacterial flora in patients may reduce the efficacy of neuraminidase inhibitor drugs during influenza virus infection
bacterial neuraminidases functions as the predominant neuraminidase when influenza virus neuraminidase is inhibited to promote the spread of infection and to inactivate the neutralization activity of saliva. Neuraminidase from bacterial flora in patients may reduce the efficacy of neuraminidase inhibitor drugs during influenza virus infection
bacterial neuraminidases functions as the predominant neuraminidase when influenza virus neuraminidase is inhibited to promote the spread of infection and to inactivate the neutralization activity of saliva. Neuraminidase from bacterial flora in patients may reduce the efficacy of neuraminidase inhibitor drugs during influenza virus infection
bacterial neuraminidases functions as the predominant neuraminidase when influenza virus neuraminidase is inhibited to promote the spread of infection and to inactivate the neutralization activity of saliva. Neuraminidase from bacterial flora in patients may reduce the efficacy of neuraminidase inhibitor drugs during influenza virus infection
bacterial neuraminidases functions as the predominant neuraminidase when influenza virus neuraminidase is inhibited to promote the spread of infection and to inactivate the neutralization activity of saliva. Neuraminidase from bacterial flora in patients may reduce the efficacy of neuraminidase inhibitor drugs during influenza virus infection
isolation of mutants from H5N1-infected patients to explain the molecular basis of resistance to oseltamivir. Mutants are resistant to oseltamivir but still strongly inhibited by zanamivir owing to an altered hydrophobic pocket in the active site of the enzyme required for oseltamivir binding
construction of highly infectious laryngotracheitis virus expressing H5 hemagglutinin and/or N1 neuraminidase and use in ocular immunization of chickens. Animals immunized with laryngotracheitis virus expressing neuraminidase N1 died after subsequent H5N1 avian influenzy virus challenge, although survival times were prolonged compared to non-vaccinated controls. In contrast, all chickens vaccinated with either laryngotracheitis virus expressing hemagglutinin H5 alone, or hemagglutinin H5 and neuramindase N1 simultaneously, survived without showing any clinical signs
construction of highly infectious laryngotracheitis virus expressing H5 hemagglutinin and/or N1 neuraminidase and use in ocular immunization of chickens. Animals immunized with laryngotracheitis virus expressing neuraminidase N1 died after subsequent H5N1 avian influenzy virus challenge, although survival times were prolonged compared to non-vaccinated controls. In contrast, all chickens vaccinated with either laryngotracheitis virus expressing hemagglutinin H5 alone, or hemagglutinin H5 and neuramindase N1 simultaneously, survived without showing any clinical signs
construction of highly infectious laryngotracheitis virus expressing H5 hemagglutinin and/or N1 neuraminidase and use in ocular immunization of chickens. Animals immunized with laryngotracheitis virus expressing neuraminidase N1 died after subsequent H5N1 avian influenzy virus challenge, although survival times were prolonged compared to non-vaccinated controls. In contrast, all chickens vaccinated with either laryngotracheitis virus expressing hemagglutinin H5 alone, or hemagglutinin H5 and neuramindase N1 simultaneously, survived without showing any clinical signs