Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.11 (CD10)
 9,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The alternative or properdin pathway of complement is primarily controlled by the endopeptidase C3b inactivator (C3bINA) and the nonproteolytic glycoprotein beta1H. The molecular mechanisms of control were investigated by performing binding studies of radiolabeled complement proteins to C3b bearing sheep erythrocytes (E(S)C3b). C3b was found to have distinct binding sites for beta1H, C3bINA, Factor B, and properdin. beta1H binding increased C3bINA binding 30-fold, while Factor B binding prevented C3bINA action on C3b and was competitive with beta1H binding. Properdin binding, which facilitates Factor B interaction with C3b, had no effect on the beta1H and C3bINA sites. Activators such as rabbit erythrocytes (E(R)) have previously been shown to interfere with the effectiveness of the control by C3bINA and beta1H, thereby allowing unrestricted formation of C3 convertase. Such restriction of control does not occur on the surface of E(S), a nonactivator of the alternative pathway. On the basis of comparative binding studies, restriction of control is explained entirely by reduced binding of beta1H to E(R)C3b relative to E(S)C3b. Access of properdin, Factor B, C3bINA, and the Fab fragment of anti-C3 to the two cell types was unrestricted. Restriction of beta1H control could be generated on the surface of E(S) by removal of cell-surface sialic acid with neuraminidase (acylneuraminyl hydrolase; EC 3.2.1.18). This enzymatic treatment converted E(S) from a nonactivator to an activator of the alternative pathway.
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PMID:Complement C3 convertase: cell surface restriction of beta1H control and generation of restriction on neuraminidase-treated cells. 27 81

Renal tumours were induced in dietary-primed rats by injection of dimethylnitrosamine. Control and tumour tissue was excised at varying periods and maintained in short-term organ culture in the presence of 3H- or 14C-fucose. The plasma membranes were then isolated, and the isotopic profiles of normal kidney and renal tumour membrane proteins were established, using polyacrylamide-gel electrophoresis in dodecyl sulphate. Several fucose-containing glycoproteins of the plasma membranes were found to alter upon neoplastic transformation: 4 increased and 3 decreased. The probable identity of 2 of these proteins is indicated: alpha-foetoprotein is one of the glycoproteins which increased, whereas neutral endopeptidase decreased in the tumour membranes. Fluorescein-labelled lectin binding by the kidney tissue was also found to alter upon transformation. The most marked changes were an increase in sialic acid (neuraminidase-sensitive) and galactosamine (Ricinus communis agglutinin Type I) in the nuclei of some neoplastic cells and some hyperplastic-tubule cells.
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PMID:Saccharide alterations in rat kidney associated with malignant transformation by injection of dimethylnitrosamine. 65

We investigated the effects of neuraminidase, a viral enzyme that cleaves alpha ketosidic cell-bound sialic acids, to see if it accounts for parainfluenza and influenza virus-induced airway hyperreactivity. Accordingly, Vibrio cholerae neuraminidase was administered intratracheally in guinea pigs, and airway reactivity was assessed 3 h later. Removal of sialic acid residues was evaluated by histologic studies. Airway responsiveness was determined in anesthetized, tracheotomized, and mechanically ventilated guinea pigs by exposing them to increasing concentrations of aerosolized bronchoconstrictor agents. Respiratory system conductance was measured by the occlusion method. Neuraminidase injected intratracheally did not change airway reactivity to 10(-4) to 10(-2) M acetylcholine or 10(-4) to 2.5 x 10(-3) M histamine; nor did it prevent aerosolized albuterol from inhibiting histamine-induced bronchoconstriction. Substance P (10(-6) to 5 x 10(-5) M) had no significant bronchoconstrictor effect on guinea pigs pretreated with saline or neuraminidase. In guinea pigs pretreated with aerosols of the neutral endopeptidase inhibitor phosphoramidon (10(-4) M) before the concentration curve to aerosolized substance P was recorded, neuraminidase significantly reduced substance P-induced bronchoconstriction. When bronchoconstriction was induced by the 4-11 fragment of substance P (10(-5) to 10(-2) M), which is devoid of positive charges, it did not differ significantly in guinea pigs pretreated with saline and those pretreated with neuraminidase. These results indicate that in the guinea pig, neuraminidase injected intratracheally does not induce non-specific airway hyperreactivity and may alter the binding of substance P to its receptors.
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PMID:Effects of neuraminidase on airway reactivity in the guinea pig. 137 96

The biosynthesis, glycosylation and subcellular localization of the neutral endopeptidase-24.11 were studied in cultured human fibroblasts. The enzyme was synthesized as a precursor (Mr 88,000) containing four or five N-linked oligosaccharides. Within 1 h the synthesis-mature (Mr 94,000) endopeptidase-24.11 was formed and contained sialylated oligosaccharides. The half-life of endopeptidase-24.11 was 3.7 days and in the presence of 10 mM-NH4Cl it increased to 6 days. Mature endopeptidase-24.11 was solubilized with 0.2% saponin and partitioned into Triton X-114. In intact fibroblasts, endopeptidase-24.11 was accessible to antibodies and to neuraminidase even when the treatment was performed at 4 degrees C. The localization of endopeptidase-24.11 to the plasma membrane in cultured fibroblasts was further demonstrated by immunocytochemistry.
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PMID:Neutral endopeptidase-24.11 (enkephalinase). Biosynthesis and localization in human fibroblasts. 348 Dec 63

The carbohydrate antigen 3-fucosyl-N-acetyl-lactosamine (FAL) is expressed on human granulocytes and is detected by a monoclonal antibody B4.3. After neuraminidase treatment, this structure can also be detected on monocytes and on the cells of nearly all acute myeloid leukemia patients (38/39). It is then also present on the cells of a number of CALLA-positive lymphatic leukemias (8/18), but not on T-ALL and B-ALL cells. On cells of patients with AUL, the antigen is then detected in many TdT+ cases, but not in TdT- cases.
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PMID:Detection of the granulocyte-specific antigen 3-fucosyl-N-acetyl-lactosamine on leukemic cells after neuraminidase treatment. 619 17

Culture supernatants of Pasteurella haemolytica A1 contain an O-sialoglycoprotein endopeptidase that cleaves human glycophorin A. This enzyme is inhibited by micromolar concentrations of Zn2+. It can be separated from a neuraminidase activity in culture supernatants by ion-exchange chromatography. The neuraminidase activity can cause the de-sialation of the bovine soluble sialoglycoprotein, fetuin. However fetuin is not cleaved proteolytically either by culture supernatants from P. haemolytica A1 or by chromatographically purified O- sialoglycoprotein endopeptidase or neuraminidase.
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PMID:The Pasteurella haemolytica O-sialoglycoprotein endopeptidase is inhibited by zinc ions and does not cleave fetuin. 860 34

We have compared the ability of human alpha/beta and gamma/delta T lymphocytes to adhere to selectin-bearing substrates, an interaction thought to be essential for homing and localization at sites of inflammation. Both T cell populations form rolling adhesions on E- and P-selectin substrates under physiologic flow conditions. Although equivalent to alpha/beta T cells in binding to E-selectin, gamma/delta T cells demonstrated greater ability to adhere to P-selectin that was purified or expressed on the surface of activated, adherent platelets. Under static conditions, 80% of gamma/delta T cells and 53% of alpha/beta T cells formed shear-resistant adhesions to P-selectin, whereas only 30% of gamma/delta and alpha/beta T cells adhered to E-selectin. The enhance ability of gamma/delta T cells to adhere to P-selectin cannot be attributed to differences in expression of the P-selectin glycoprotein ligand (PSGL-1), as all alpha/beta T cells versus approximately 75% of gamma/delta T cells expressed PSGL-1. Both cell populations expressed a similar percentage of the carbohydrate antigens sialyl LewisX and cutaneous lymphocyte-associated antigen. Depletion of lymphocyte populations or T cell clones bearing these oligosaccharides with the monoclonal antibody CSLEX-1 and HECA-452, respectively, resulted in a substantial reduction in adhesion to E-selectin and slight reduction in adhesion to P-selectin under flow conditions. Treatment of cells with an endopeptidase that selectively degrades O-sialomucins such as PSGL-1, abolished P-selectin but not E-selectin adhesion. Removal of terminal sialic acids with neuraminidase or protease treatment of cells abrogated cell adhesion to both selectin substrates. These results provide direct evidence for the presence of distinct E- and P-selectin ligands on T lymphocytes and suggest that gamma/delta T cells may be preferentially recruited to inflammatory sites during the early stages of an immune response when P-selectin is upregulated.
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PMID:Interactions of human alpha/beta and gamma/delta T lymphocyte subsets in shear flow with E-selectin and P-selectin. 864 61

The development of plasmid-based rescue systems for influenza virus has allowed previous studies of the neuraminidase (NA) virion RNA (vRNA) promoter to be extended, in order to test the hypothesis that alternative base pairs in the conserved influenza virus vRNA promoter cause attenuation when introduced into other gene segments. Influenza A/WSN/33 viruses with alternative base pairs in the duplex region of the vRNA promoter of either the polymerase acidic (PA) or the NS (non-structural 1, NS1, and nuclear export, NEP, -encoding) gene have been rescued. Virus growth in MDBK cells demonstrated that one of the mutations, the D2 mutation (U-A replacing G-C at nucleotide positions 12'-11), caused significant virus attenuation when introduced into either the PA or the NS gene. The D2 mutation resulted in the reduction of PA- or NS-specific vRNA and mRNA levels in PA- or NS-recombinant viruses, respectively. Since the D2 mutation attenuates influenza virus when introduced into either the PA or the NS gene segments, or the NA gene segment, as demonstrated previously, this suggests that this mutation will lead to virus attenuation when introduced into any of the eight gene segments. Such a mutation may be useful in the production of live-attenuated viruses.
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PMID:Alternative base pairs attenuate influenza A virus when introduced into the duplex region of the conserved viral RNA promoter of either the NS or the PA gene. 1260

Although the important role of the non-structural (NS1 and NEP) gene of influenza A in virulence of the virus is well established, our knowledge about the extent of variation in the NS gene pool of influenza A viruses in their natural reservoirs in Kazakhstan is incomplete. 17 influenza A viruses of different subtypes were studied in this paper. Seven types of haemagglutinin and five different neuraminidase subtypes in eight combinations were found among the isolated viruses. A comparison of nucleotide sequences of isolated viruses revealed a substantial number of silent mutations, which results in high degree of homology in amino acid sequences. By phylogenetic analysis it was shown that two distinct gene pools, corresponding to both NS allele A with 5 Clades and B, were present at the same time in Kazakhstan. The degree of variation within the alleles was very low. In our study allele A viruses had a maximum of 5% amino acid divergence in Clade while allele B viruses had only 4% amino acid divergence.
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PMID:Phylogenetic analysis of the non-structural (NS) gene of influenza A viruses isolated in Kazakhstan in 2002-2009. 2433 80

In total 1,525 blood serum samples were collected in October, 2013 in Russian Asia from people who reside in territories that are at high risk for emergence of influenza viruses with pandemic potential. Presence of antibodies to influenza viruses in the sera was tested in hemagglutination inhibition test. None of the samples produced positive results with the antigens A/H5 and A/H7. Twelve strains of influenza A(H1N1pdm09) virus were isolated from people who died presumably from influenza during 2013-2014 epidemic season. All strains were similar to vaccine strain A/California/07/09 according to their antigenic properties and sensitivity to anti-neuraminidase drugs (oseltamivir and zanamivir). Genetic analysis revealed that all strains belong to group 6, subgroup 6B of influenza A(H1N1)pdm09 virus. Substitutions in HA1: S164F add E235K as well as E47G, A86V, K331R, N386K, N397K in NA, and K131E, N29S in NS1, and N29S, R34Q in NEP separate investigated strains into two groups: 1st group-A/Chita/1114/2014, A/Chita/1115/2014, A/Chita/853/2014, A/Barnaul/269/2014 and 2nd group-A/Chita/655/2014, A/Chita/656/2014, A/Chita/709/2014, A/Chita/873/2014. Mutation D222G in HA1, which is often associated with high morbidity of the illness, was present in strain A/Novosibirsk/114/2014. Substitution N386K in NA removes a potential N-glycosylation site in neuraminidases of A/Chita/1114/2014, A/Chita/1115/2014, A/Chita/853/2014, A/Barnaul/269/2014, A/Novosibirsk/114/2014, and A/Blagoveshensk/252/2014.
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PMID:Herd immunity and fatal cases of influenza among the population exposed to poultry and wild birds in Russian Asia in 2013-2014. 2610 90


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