Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.2.1.23 (beta-galactosidase)
14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human adult lung fragments removed from macroscopically undamaged and anthracosis exempted zones of lungs of 20 pneumonectomies made for cancer, were tested for 25 enzymic activities. The location and intensities of these enzymic activities were different in the lung tissue components; The bronchial epithelia contained highly active LDH, MDH, SDH, NADH-TR and NADPH-TR, glucose-6-phosphate dehydrogenase, active hydroxyproline-2-epimerase, alkaline phosphatase. Ca2+-activated ATP-ase, and beta-galactosidase. Bronchial and vascular muscles presented intense activities of LDH, MDH and SDH of alkalinephosphatase, AMP-ase and Ca2+-activated ATP-ase, as well as of beta-galactosidase. The alveolar walls presented high activities of SDH, MDH and LDH, of alkaline and acid phosphatases, of beta-galactosidase and of Tween-40 and 60-esterases, of HEP, cytochrome-oxidase and peroxidase. The free alveolar macrophages were active for LDH, MDH, SDH, NADH-TR and NADPH-TR, G1-6-ph-DH, acid and alkaline phosphatase, cytochrome-oxidase and peroxidase, HEP, AMP-ase and Mg2+-activated ATP-ase, Tween-esterases, naphthol-ASD-acetate esterase, and beta-galactosidase. The endothelia contained high activities of alkaline phosphatase, of AMP-ase and Mg2+-activated ATPase, of LDH, MDH and SDH, and of beta-galactosidase. In bronchial lymphoid nodules it was the LDH, MDH, SDH, cytochrome-oxidase and peroxidase, HEP, alkaline phosphatase and AMP-ase, Tween-60-esterase and beta-galactosidase that were active. The interlobular areas of the lung presented intense activities of SDH, MDH, LDH, HEP and cytochrome-oxidase. The activities of the other tested enzymes were weaker or absent in the adult human lung components, the same as those of aminopeptidases which were present only in some free alveolar macrophages. The discussion of some relationships between these enzymic actitivies and the morphology of the human adult lung tissue asserted that the latter could not be considered as a "normal" tissue but as one overstrained by the components of blood and polluted air.
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PMID:Histoenzymology of the lung. I. Enzyme activities of the lung tissue of acult humans; relationships between structure and functions. 14 Mar 14

This work is part of an investigation into G. I. mucin susceptibility to enzyme degradation in normal and disease states. Formalin-fixed/paraffin embedded foetal (14-23 weeks) and neonatal colonic tissue was stained for mucins (neutral, N- and O-acylated sialomucins and sulphomucins) and PNA, UEA1, and Limax flavus. Enzymes tested: neuraminidases, alpha- and beta-galactosidase (E. coli and B. testis), beta-N-acetyl-glucosaminidase, alpha-fucosidase, single or in sequence, with and without prior neuraminidase treatment and followed by the stains. Acid mucins predominate throughout foetal life, sulphation occurs at 14 weeks and O-acylated sialomucins at 23 weeks. PNA and UEA1 are seen in traces or not detected. The mucin profile at birth is similar to the adult. Colonic mucins are susceptible to neuraminidase which abolishes Limax staining. The glycosidases effect on PNA is seen only with prior neuraminidase treatment and is particularly marked with beta-Gal(BT) in Neu----beta-Gal----beta-N-AcetylGlc than with beta-Gal (EC). Fucosidase with prior neuraminidase treatment has effect on UEA1 (decreases) and PNA (increases) affinities. Neuraminidase is essential as a first step in the process and by using beta-galactosidases EC and BT it was possible to show different PNA binding affinities. Preliminary data demonstrate the feasibility of this histochemical approach to the study of colonic mucins and forms the basis for further studies in the adult.
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PMID:Goblet cell mucin in human foetal colon, its composition and susceptibility to enzyme degradation: a histochemical study. 264 9

We have studied the physiological effects of mitomycin C induction on cells carrying ColE1 plasmids with differing configurations of three genes: the structural gene coding for colicin (cea), a gene responsible for mitomycin C lethality (kil) that we located as part of an operon with cea, and the immunity (imm) gene, which lies near cea but is not in the same operon. kil is close to or overlaps imm. When cea(+) plasmids are present mitomycin C induction results in 100-fold or greater increases in the level of colicin. Within an hour after induction more than 90% of cells carrying cea(+)kil(+) plasmids are killed and macromolecular synthesis stops, capacity for transport of proline, thiomethyl beta-D-galactoside, and alpha-methyl glucoside is lost, and the membrane becomes abnormally permeable as indicated by an increased accessibility of intracellular beta-galactosidase to the substrate o-nitrophenyl beta-D-galactoside. All of these events occur when a cea(-)kil(+)imm(+) plasmid is present and none does when the plasmid is cea(+)kil(-)imm(+), so the damage can be attributed solely to the Kil function and not to the presence of colicin. However, cells carrying a cea(+)kil(-)imm(-) plasmid are killed upon induction, apparently by action of endogenous colicin on the nonimmune cytoplasmic membrane. The pattern of accompanying physiological damage is distinguished from the kil(+)-associated damage by an enhancement of alpha-methyl glucoside uptake and accumulation and efflux of alpha-methyl glucoside 6-phosphate and by an absence of the alteration in membrane permeability for o-nitrophenyl beta-D-galactoside. These features are typical of colicin E1 action on the membrane. The induced damage is not prevented by trypsin and occurs in cells of a strain specifically tolerant to exogenous colicin E1, indicating that the attack is from inside the cell.
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PMID:Alternative forms of lethality in mitomycin C-induced bacteria carrying ColE1 plasmids. 640 39

beta-Galactosidase was normalized by a serine-thiol protease inhibitor, leupeptin with concentration of 10 micrograms/ml in cultured skin fibroblasts from patients with beta-galactosidase-alpha-neuraminidase deficiency (beta-Gal-/Neu-). The induction of this enzyme was not observed in normal cells. Because the enzymic activity of cathepsin B1 increased significantly both in beta-Gal-/Neu- and normal cells by leupeptin loading, the restoration of beta-galactosidase in beta-Gal-/Neu- cells can not be explained by the theory that leupeptin inhibited intracellular degradation of beta-galactosidase molecules. The effects of leupeptin and sucrose on lysosomal hydrolase induction were compared.
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PMID:Induction of beta-galactosidase in beta-galactosidase-alpha-neuraminidase deficiency: effects of leupeptin and sucrose. 643 25

The outer surface of mouse B lymphocytes carries constitutive and inducible beta-galactosidase isozymes. A brief (30 min) treatment of B lymphocytes with lysophosphatidylcholine (lyso-Pc) immediately induced an approximate 3-fold higher beta-galactosidase activity than the constitutive isozyme of untreated B lymphocytes. Thus, the lyso-Pc-inducible isozyme is not a de novo enzyme. Outer surface of mouse T lymphocytes carries constitutive (non-Neu-1) and inducible (Neu-1) sialidase isozymes. The lyso-Pc-inducible beta-galactosidase of B lymphocytes and the Neu-1 sialidase of T lymphocytes were required for conversion of vitamin D3-binding protein (Gc protein) to a potent macrophage activating factor. This enzymatic generation of the macrophage activating factor was mediated via enzyme-associated receptors.
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PMID:Roles of beta-galactosidase of B lymphocytes and sialidase of T lymphocytes in inflammation-primed activation of macrophages. 772 26

We evaluated the ability of a replication-deficient, recombinant adenoviral vector to transfer the bifunctional gene GAL-TEK, which expresses a marking/therapeutic gene product, to naturally occurring cat fibrosarcomas in situ. GAL-TEK contains an in-frame fusion of the bacterial LacZ gene for histochemical marking of tumors with beta-galactosidase (beta-Gal) and the HSV tk gene for enzyme-prodrug activation of the prodrug ganciclovir (GCV) to induce selective tumor cell killing. GAL-TEK bifunctional marking and cell killing activities were tested in vitro after adenoviral vector infection of HT1080 human fibrosarcoma cells. The tk activity of GAL-TEK is shown to be almost as potent as HSV tk to catalyze conversion of GCV to GCV nucleotides and promote selective cell killing. Using 8 cats with recurring 2.5-cm2 fibrosarcomas that either arose spontaneously or were induced by vaccine, we determined experimentally the administration routes and times required for optimum GAL-TEK gene transfer by beta-Gal histological staining and reverse transcriptase polymerase chain reaction to the multiple compartments of the growing fibrosarcomas consonant with minimizing collateral infection of neighboring tissues and other unwanted side effects.
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PMID:In vivo marking of spontaneous or vaccine-induced fibrosarcomas in the domestic house cat, using an adenoviral vector containing a bifunctional fusion protein, GAL-TEK. 852 80

When rat peritoneal nonadherent cells were treated with inflammatory lipid metabolites and cultured with adherent cells in 1% fetal calf serum (FCS) supplemented medium RPMI 1640 (FCS medium) for 3 hr, markedly enhanced phagocytic and superoxide generating capacities of macrophages were observed. Stepwise preparation of conditioned medium of lysophosphatidylcholine (lyso-Pc)-treated B cells and untreated T cells in FCS medium generated a potent macrophage activating factor whereas cultivation of lyso-Pc-treated B cells alone in a 1% adult rat serum supplemented medium efficiently generated the macrophage activating factor. Generation of macrophage activating factor requires a precursor protein, serum vitamin D3-binding protein (DBP), as well as participation of lymphocyte glycosidases. The lyso-Pc-inducible beta-galactosidase of B lymphocytes and the Neu-1 sialidase of T lymphocytes modified bovine DBP (bDBP) to yield the macrophage activating factor, a protein with N-acetylgalactosamine as the remaining sugar. In contrast, lyso-Pc-inducible beta-galactosidase of B cells alone modified rat DBP (rDBP) to yield the macrophage activating factor, a protein with N-acetylgalactosamine as the remaining sugar. Thus, we conclude that bDBP carries a trisaccharide composed of N-acetylgalactosamine, galactose, and sialic acid while rDBP carries a disaccharide composed of N-acetylgalactosamine and galactose.
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PMID:Vitamin D3-binding protein as a precursor for macrophage activating factor in the inflammation-primed macrophage activation cascade in rats. 866 Aug 14

When mouse peritoneal nonadherent (lymphocytes) cells were treated with lysophosphatidylcholine (lyso-Pc) and cultured with adherent cells (macrophages) in 1% fetal calf serum (FCS)- or adult mouse serum (AMS)-supplemented medium for 3 h, markedly enhanced phagocytic and superoxide-generating capacities of macrophages were observed. Stepwise cultivation of lyso-Pc-treated B cells and untreated T cells with an FCS-supplemented medium generated a macrophage-activating factor (MAF), whereas cultivation of lyso-Pc-treated B cells alone in AMS-supplemented medium was sufficient to generate the MAF. The accumulated evidence suggests that lyso-Pc-inducible beta-galactosidase of B lymphocytes and the Neu-1 sialidase of T lymphocytes modified the bovine serum vitamin D3-binding protein (DBP) to yield the MAF, a protein with N-acetylgalactosamine as the remaining sugar. In contrast, the lyso-Pc-inducible beta-galactosidase of B cells alone modified mouse DBP to yield the MAF. These observations led us to conclude that bovine DBP carries a trisaccharide composed of N-acetylgalactosamine, galactose, and sialic acid, whereas mouse DBP carries a disaccharide composed of N-acetylgalactosamine and galactose. Thus, macrophages of a T-cell-deficient nude (BALB/c nu/nu) mouse and a T-cell Neu-1 sialidase-deficient SM/J mouse were efficiently activated by administration of lyso-Pc.
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PMID:Role of vitamin D3-binding protein in activation of mouse macrophages. 875 64

In order to exploit the tumour-specific nature of ERBB2 expression for genetic prodrug-activation therapy, we have generated recombinant adenoviral, retroviral and plasmid vectors containing an expression cassette consisting of the ERBB2 promoter and herpes simplex virus thymidine kinase coding sequence. In the case of the adenoviral vectors, the expression cassette was introduced into the E1 or E3 region of the genome. All of the vectors were capable of sensitizing ERBB2-positive cells to the action of ganciclovir. In contrast to the retroviral and plasmid vectors, however, transduction with the adenoviral vectors also resulted in sensitization of ERBB2-negative cells to ganciclovir, infection of cell lines with a beta-galactosidase expressing adenovirus showed that the sensitizing effect was not due to adenoviral infection per as in all but one of the cell lines tested. This study demonstrates that the ERBB2 promoter can be used to induce ERBB2-dependent sensitization to ganciclovir when in the context of retroviral and plasmid vectors. Observations made in this study do, however, suggest that adenoviral vectors may not be the ideal system to engineer conditional expression, and possible explanation for this phenomenon are discussed.
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PMID:Suicide gene expression induced in tumour cells transduced with recombinant adenoviral, retroviral and plasmid vectors containing the ERBB2 promoter. 898 36

Sodium valproate (VPA), a simple branched-chain fatty acid that has anticonvulsant activity and is used in the treatment of many forms of epilepsy, has been reported to stimulate human immunodeficiency virus (HIV) type 1 replication in acutely infected CEM and chronically infected U1 cells (Chemico-Biological Interactions 1994;91:111-121). When attempting to reproduce and extend these findings, we confirmed that VPA is able to stimulate HIV-1(IIIB) replication in acutely infected CEM and C8166 T lymphocytic cell lines and chronically infected ACH-2 and U937/IIIB/LAI cells in a concentration-dependent manner. The stimulatory effect of VPA on HIV replication in CEM cells was not increased by pretreatment of the cells with VPA for 24 hr before infection. However, we could not detect any stimulatory effect of VPA on HIV-1(IIIB) replication in acutely infected peripheral blood mononuclear cells (PBMCs), MT-4, MT-2, HUT-78, and MOLT-4 (clone 8) cells and in chronically infected HUT-78/IIIB/LAI cells. The stimulatory effect by VPA under certain conditions (see above) may be ascribed to an enhanced HIV transcription, as VPA was found to enhance the HIV long terminal repeat (LTR)-directed expression of beta-galactosidase in transiently transfected HLtat, P4, and COS7 cells. VPA did not enhance beta-galactoside expression mediated by the cytomegalovirus (CMV) promoter. VPA did not affect HIV-induced syncytium formation. Nor had VPA any direct inactivating effect on HIV.
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PMID:Cell type-dependent effect of sodium valproate on human immunodeficiency virus type 1 replication in vitro. 900 4


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