Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.23 (beta-galactosidase)
 14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Brush borders were prepared from pig intestinal mucosa and the membrane proteins solubilized with either Triton X-100 or papain. Proteins, thus released, were used as antigens to raise antisera in rabbits. The immunoglobulin G fractions were isolated and shown by the double layer immunofluorescence staining technique to react only with the brush border region of the enterocyte. The antibodies obtained were used in immunoelectrophoretic studies on the brush border proteins. Eight hydrolytic activities were identified by the use of histo-chemical staining methods. These were the microsomal aminopeptidase (EC 3.4.11.2), aspartate aminopeptidase (EC 3.4.11.7), dipeptidyl peptidase IV (EC 3.4.14.X), lactase (EC 3.2.1.23), glucoamylase (EC 3.2.1.3), sucrase (EC 3.2.1.48), isomaltase (EC 3.2.1.10) and alkaline phosphatase (EC 3.1.3.1). In addition, at least four faint immunoprecipitates were formed but none of these were identified.
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PMID:Immunoelectrophoretic studies on pig intestinal brush border proteins. 2 Sep 74

The enzymic activity of acid alkaline phosphatases, of alanyl- and leucine-aminopeptidases, of beta-galactosidase and beta-glucuronidase, and of Tween-60-esterase was tested in the rabbit lung tissue during the following experimental processes: a) the sensitization with Freund adjuvant containing PPD and challenge of the delayed hypersensitivity reaction to PPD), b) the sensitization with gamma-globulin in Freund adjuvant, c) the pulmonary Arthus reaction, d) the lung granulomas induced by intravenous administration of Freund adjuvant containing heterologous lung proteins, e) the tuberculosis and silicotuberculosis under the influence of tuberculostatics. A metabolic intensification expressed by a marked increase of the tested hydrolytic enzymes was observed comparatively with controls in all these immune, granulomatous and inflammatory processes experimentally induced in the lung. The morphologic substrate of this behaviour was represented by the numerous cell proliferation and differentiations of the reticulomacrophagic type occurring during these experimental processes under the stimulation of antigenic elicitors. The latter also induced an increase of the lysosome-formation as submicroscopic site of these hydrolytic enzymes.
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PMID:Histoenzymology of the lung. II. The behaviour of lung hydrolytic enzymes during some experimental pulmonary processes. 14 Mar 19

A brush-border-specific antiserum was raised in rabbits, with Triton X-100-solubilized brush border proteins from pig intestine being used as antigens. The antiserum was used in immunoelectrophoretic studies of brush border proteins solubilized with Triton X-100. Five immunoprecipitates were obtained which corresponded to microsomal aminopeptidase (EC 3.4.11.2), asparate aminopeptidase (EC 3.4.11.7), lactase (beta-galactosidase, EC 3.2.1.23), maltase (exo-1,4-alpha-glucosidase, EC 3.2.1.3) and sucrase-isomaltase (sucrose alpha-glucohydrolase, EC 3.2.1.48). A faint immunoprecipitate was also found for the glycylprolyl dipeptidyl peptidase (EC 3.4.14.-). The brush border proteins were solubilized on a large scale from a brush border membrane preparation by the use of Triton X-100; the peptidases obtained were homogeneous in size and had hydrophobic properties. By chromatography on columns of concanavalin A-Sepharose, hydroxyapatite, Ultrogel AcA 34, DEAE-cellulose and immunosorbent, gamma-glutamyl transpeptidase (gamma-glutamyl transferase, EC 2.3.2.2) and microsomal aminopeptidase were each isolated in separate fractions. Glycylprolyl dipeptidyl peptidase and asparate aminopeptidase were obtained in another fraction. Immunoelectrophoretic, inhibitor and chromatographic studies showed that the intestinal brush border peptidases are similar to the corresponding particulate peptidases obtained from other organs.
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PMID:Intestinal brush border peptidases. 24 83

Cyclosporin (CsA) is an immunosuppressant which binds to cyclophilin (Cyp). The relationship between Cyp binding and immunosuppression has been questioned since one of the analogs of CsA, N-methyl-L-alanyl6 cyclosporin (methyl-alanyl CsA) binds to Cyp but is not immunosuppressive. We compared the immunosuppressive properties of CsA, methyl-alanyl CsA and o-acetyl-threonine2 cyclosporin (monoacetyl CyC), since monoacetyl CyC does not bind to Cyp when tested in cell-free assays and its immunosuppressive properties had not been tested. Cyp is a peptidyl-prolyl isomerase which is abundant in all human tissues, yet the activities of CsA are mostly confined to inhibition of T cell and thymocyte activation, and to neuro- and nephro-toxicity and are independent of inhibition of the isomerase. Activation of thymocytes and of T cells is regulated by the binding of a nuclear factor(s) (NFs) to the NF-AT region (-285 to -255) of the IL-2 promoter. We studied inhibition of binding to the NF-AT region of NFs derived from primary cultures of thymocytes treated with CsA or its analogs. In addition, we compared the effect of CsA and its analogs on the expression of the IL-2 gene in a stably transfected Jurkat-cell line (Fgl 5) which contains three copies of NF-AT and the reporter enzyme beta-galactosidase; and on inhibition of proliferation induced by concanavalin A (Con A) or IL-2. We found that monoacetyl CyC which does not bind to Cyp is immunosuppressive by our criteria when tested in cultured cells due to either a different mechanism of action or to metabolic activation.
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PMID:Comparison of the properties of the CsA analogs monoacetyl CyC (o-acetyl-threonine2 cyclosporin) and methyl-alanyl CsA (N-methyl-L-alanyl6 cyclosporin); monoacetyl cyclosporin is immunosuppressive without binding to cyclophilin. 162 22

Gamma-Glutamyl transpeptidase (gamma-GT) was studied histochemically and biochemically in the rat epididymis after castration with or without testosterone treatment, or after hemicastration and ligation of the efferent ducts. There was a strong reaction to gamma-GT in the apical part of the epithelium in the caput epididymis, while in the corpus and cauda the reaction was confined mainly to the luminal contents. Castration caused a marked decline in epithelial gamma-GT activity within 10 days. Subsequent testosterone treatment (1 mg/day for 10 days) restored gamma-GT activity in the apical surface and lumen. After hemicastration of adult rats, and after hemicastration or ligation of the efferent ducts in immature 28-day-old rats, a small but significant (P less than 0.001) decrease was observed in gamma-GT activity in the epididymal caput compared to controls. The quantities of six other enzymes (beta-N-acetylglucosaminidase, beta-galactosidase, angiotensin-converting enzyme, alanyl amino-peptidase, dipeptidyl peptidase IV, acid phosphatase) also displayed significant changes after castration and restoration of activities by testosterone treatment. However, their distribution in the caput and cauda epididymis was more even than that of gamma-GT, and the changes after castration were less drastic. It is concluded that gamma-GT is a highly sensitive androgen-dependent secretory marker in the caput epididymis and may have an important function in sperm maturation.
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PMID:Gamma-glutamyl transpeptidase in rat epididymis: effects of castration, hemicastration and efferent duct ligation. 257 65

In gram-positive bacteria, HPr, a phosphocarrier protein of the phosphoenolpyruvate:sugar phosphotransferase system (PTS), is phosphorylated by an ATP-dependent, metabolite-activated protein kinase on seryl residue 46. In a Bacillus subtilis mutant strain in which Ser-46 of HPr was replaced with a nonphosphorylatable alanyl residue (ptsH1 mutation), synthesis of gluconate kinase, glucitol dehydrogenase, mannitol-1-P dehydrogenase and the mannitol-specific PTS permease was completely relieved from repression by glucose, fructose, or mannitol, whereas synthesis of inositol dehydrogenase was partially relieved from catabolite repression and synthesis of alpha-glucosidase and glycerol kinase was still subject to catabolite repression. When the S46A mutation in HPr was reverted to give S46 wild-type HPr, expression of gluconate kinase and glucitol dehydrogenase regained full sensitivity to repression by PTS sugars. These results suggest that phosphorylation of HPr at Ser-46 is directly or indirectly involved in catabolite repression. A strain deleted for the ptsGHI genes was transformed with plasmids expressing either the wild-type ptsH gene or various S46 mutant ptsH genes (S46A or S46D). Expression of the gene encoding S46D HPr, having a structure similar to that of P-ser-HPr according to nuclear magnetic resonance data, caused significant reduction of gluconate kinase activity, whereas expression of the genes encoding wild-type or S46A HPr had no effect on this enzyme activity. When the promoterless lacZ gene was put under the control of the gnt promoter and was subsequently incorporated into the amyE gene on the B. subtilis chromosome, expression of beta-galactosidase was inducible by gluconate and repressed by glucose. However, we observed no repression of beta-galactosidase activity in a strain carrying the ptsH1 mutation. Additionally, we investigated a ccpA mutant strain and observed that all of the enzymes which we found to be relieved from carbon catabolite repression in the ptsH1 mutant strain were also insensitive to catabolite repression in the ccpA mutant. Enzymes that were repressed in the ptsH1 mutant were also repressed in the ccpA mutant.
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PMID:Loss of protein kinase-catalyzed phosphorylation of HPr, a phosphocarrier protein of the phosphotransferase system, by mutation of the ptsH gene confers catabolite repression resistance to several catabolic genes of Bacillus subtilis. 819 89

The previously detected ebony (e) locus (Caizzi et al., 1987) consists of a complex gene structure that is divided into seven exons. An open reading frame encoding the putative Ebony protein of 98.5 kDa exhibits homology to a family of peptide synthetases (Stachelhaus and Marahiel, 1995), in good correlation with the proposed function as beta-alanyl-dopamine synthetase. Multiple ebony transcripts are detected throughout development. P-factor mediated transformation of genomic DNA rescues the cuticle, electrophysiological and behavioural phenotypes. Fusion of the ebony reading frame with that of beta-galactosidase of E. coli reveals expression in cuticle and nervous system. Strong staining in the first and, to a lesser extent, in the second optic neuropile may reflect the pronounced visual defect observed in ebony mutants. In addition, weak central brain and thoracic ganglion expression is detected in flies. Conservation of a multidomain protein structure known from peptide synthetases should have functional implications on the putative reaction mechanism of peptide bond formation.
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PMID:The Drosophila ebony gene is closely related to microbial peptide synthetases and shows specific cuticle and nervous system expression. 985 43

1. The studies were carried on 98 random 6-week-old male mice. The mice were divided into control and experimental groups. The experimental animals were given 10% and 20% ethanol solution daily for 7, 14 and 28 days. 2. In the lysosomal fractions of the liver, kidneys, muscle and brain, the activities of beta-galactosidase, beta-glucuronidase, N-acetyl-beta-glucosaminidase, alanyl-aminopeptidase, leucyl-aminopeptidase, lysosomal esterase and lysosomal lipase were affected. 3. The changes in enzyme activities in the investigated tissue were related to the time and concentration of the administered ethanol.
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PMID:Effect of ethanol administration on activities of some lysosomal hydrolases in the mouse. 988 70

In this study, we investigated the in vivo role of adiponectin, an adipocytokine, on the development of atherosclerosis in rabbits mainly using adenovirus expressing adiponectin gene (Ad-APN) and intravascular ultrasonography. Serum adiponectin concentrations in rabbits after Ad-APN local transfer to abdominal aortas increased about nine times as much as those before transfer (P < 0.01), about ten times as much as the levels of endogenous adiponectin in adenovirus expressing beta-galactosidase gene (Ad-beta gal) treated rabbits (P < 0.01), and about four times as much as those in the aorta of non-injured rabbits on a normal cholesterol diet (P < 0.01). Ultrasonography revealed a significantly reduced atherosclerotic plaque area in abdominal aortas of rabbits infected through intima with Ad-APN, by 35.2% compared with the area before treatment (P < 0.01), and by 35.8% compared with that in Ad-beta gal-treated rabbits (P < 0.01). In rabbits infected through adventitia, Ad-APN treatment reduced plaque area by 28.9% as compared with the area before treatment (P < 0.01) and 25.6% compared with that in Ad-beta gal-treated rabbits (P < 0.01). Adiponectin significantly suppressed the mRNA expression of vascular cell adhesion molecule-1 (VCAM-1) by 18.5% through intima transfer (P < 0.05) and 26.9% through adventitia transfer (P < 0.01), and intercellular adhesion molecule-1 (ICAM-1) by 40.7% through intima transfer (P < 0.01), and 30.7% through adventitia transfer (P < 0.01). However, adiponectin had no effect on the expression of types I and III collagen. These results suggest that local adiponectin treatment suppresses the development of atherosclerosis in vivo in part by attenuating the expression of VCAM-1 and ICAM-1 in vascular walls.
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PMID:Local adiponectin treatment reduces atherosclerotic plaque size in rabbits. 1740 Aug 11

There is an association between obesity and heart failure associated with LV dysfunction. Adiponectin is an adipocyte-derived hormone that is downregulated in obesity. Here, we examined the role of adiponectin in cardiac remodeling after myocardial infarction with loss- and gain-of-function genetic manipulations in an experimental model. Myocardial infarction was created in adiponectin-deficient (APN-KO) and wild-type (WT) mice by the permanent ligation of the left anterior descending (LAD) artery. For some experiments, adenoviral vectors expressing adiponectin or beta-galactosidase were delivered systemically. Cardiac structure and function were assessed by echocardiographic and Millar catheter measurements. Myocardial capillary density was assessed by staining with anti-CD31 antibody. Myocyte apoptotic activity was determined by TUNEL-staining. Myocardial interstitial fibrosis was evaluated by Masson's trichrome staining. APN-KO mice showed exacerbated left ventricular (LV) dilation, myocyte hypertrophy and contractile dysfunction compared with WT mice at 4 weeks after LAD ligation. Impaired LV function in APN-KO mice was coupled to myocyte hypertrophy, increased apoptotic activity and interstitial fibrosis in the remote zone, and reduced capillary density in the infarct border zone. No difference in infarct size was observed between WT and APN-KO mice. Administration of adenovirus-mediated adiponectin in WT mice resulted in decreased LV dilatation and improved LV function that was associated with increased capillary density in the infarct border zone and decreased myocyte hypertrophy, diminished myocardial apoptosis and decreased interstitial fibrosis in the remote zone. These data suggest that adiponectin protects against the development of systolic dysfunction after myocardial infarction through its abilities to suppress cardiac hypertrophy and interstitial fibrosis, and protect against myocyte and capillary loss.
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PMID:Adiponectin protects against the development of systolic dysfunction following myocardial infarction. 1749 64


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