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)

The proteinuria rate and the relative clearances of beta 2-microglobulin, orosomucoid, albumin, transferrin and IgG were measured in forty-two workers exposed to cadmium and in seventy-seven control workers. A tubular type proteinuria with an increased excretion of beta 2-microglobulin and often also a glomerular type proteinuria with an increased excretion of orosomucoid, albumin, transferrin and IgG were observed mainly in workers exposed to cadmium for more than 25 years and whose cadmium concentration in blood exceeded 1 microgram Cd/100 ml and that in urine 10 microgram Cd/g creatinine. The glomerular dysfunction was also suggested by an increased plasma level of beta 2-microglobulin and creatinine. Both tubular and glomerular impairments occurred with the same prevalence and were not necessarily associated. The increased release of beta-galactosidase by the kidney suggested that cadmium can damage some epithelial cells.
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PMID:Renal excretion of proteins and enzymes in workers exposed to cadmium. 11 May 96

The czcR gene, one of the two control genes responsible for induction of resistance to Co2+, Zn2+, and Cd2+ (czc system) in the Alcaligenes eutrophus plasmid pMOL30, was cloned and characterized. The 1,376-bp sequence upstream of the czcCBAD structural genes encodes a 41.4-kDa protein, the czcR gene product, transcribed in the opposite direction of that of the czcCBAD genes. The putative CzcR polypeptide (355 amino acid residues) contains 11 cysteine and 14 histidine residues which might form metal cation-binding sites. A czcC::lacZ reporter gene translational fusion was constructed, inserted into plasmid pMOL30 in A. eutrophus, and expressed under the control of CzcR. Zn2+, Co2+, and Cd2+, as well as Ni2+, Cu2+, Hg2+, and Mn2+ and even Al3+, served as inducers of beta-galactosidase activity. Besides the CzcR protein, the membrane-bound CzcD protein was essential for induction of czc. The CzcR and CzcD proteins display no sequence similarity to two-component regulatory systems of a sensor and a response activator type; however, CzcD has 34% identity with the ZRC-1 protein, which mediates zinc resistance in Saccharomyces cerevisiae (A. Kamizomo, M. Nishizawa, Y. Teranishi, K. Murata, and A. Kimura, Mol. Gen. Genet. 219:161-167, 1989).
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PMID:CzcR and CzcD, gene products affecting regulation of resistance to cobalt, zinc, and cadmium (czc system) in Alcaligenes eutrophus. 145 58

Urinary excretion of lactate dehydrogenase (LDH), glutathione-S-transferase (GST), leucine arylamidase (LAS), gamma-glutamyltransferase (GGT), beta-galactosidase (GAL), beta-N-acetyl-D-glucosaminidase (NAG), sodium, and glucose were determined in female Sprague-Dawley rats the subsequent three days after intraperitoneal treatment with single doses of 4.5 mg CdCl2 X 1H2O/kg, 20 mg Na2CrO4/kg, and 0.75 mg HgCl2/kg body weight. Although the pathological effects were localized within the same part of the nephron (i.e., the proximal tubule), there were marked differences with regard to the extent and time course of the parameters affected. Treatment with cadmium resulted essentially in a marked decline in sodium and glucose excretion. The administration of chromate led to a slightly to moderately elevated excretion of the enzyme activities measured with the cytosolic LDH as the most increased enzyme (ca. 500% of controls on Day 3 postadministration). Median glucose excretion was unaffected whereas sodium excretion was transiently reduced. The maximum of enzyme excretion after HgCl2 was essentially the same on the first day postadministration and the amount of enzyme activity in urine up to 20 times higher compared to that after chromium. Sodium excretion was below that of controls on Days 2 and 3, whereas glucose excretion was markedly elevated (up to 8000% of controls). The results indicate that it is possible to discriminate with the use of selected urinary enzymes, substrates, and electrolytes various kinds of nephrotoxic actions not only in different but also within the same part of the nephron.
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PMID:Comparative investigations on the effects of acute intraperitoneal cadmium, chromium, and mercury exposure on the kidney. 287 41

We have characterized the UDP-galactose: alpha-N-acetylgalactosaminide beta 3 galactosyltransferase in human tracheal epithelium using asialo ovine submaxillary mucin as the acceptor. Maximal enzyme activity was obtained at pH 6.0-7.5 and at 20-25 mM MnCl2 and at 2% Triton X-100. Cd2+ could substitute for Mn2+ as the divalent ion cofactor. Spermine, spermidine, putrecine, cadaverine, and poly-L-lysine stimulated the enzyme activity at low (2.5 mM) MnCl2 concentration. The apparent Michaelis constants for N-acetylgalactosamine, asialo ovine submaxillary mucin, and UDP-galactose were 15.5, 1.14, and 1.36 mM, respectively. The enzyme activity was not affected by alpha-lactalbumin. The alpha-N-acetygalactosaminide beta 3 galactosyltransferase was shown to be different from the N-acetylglucosamine galactosyltransferase by acceptor competition studies. The product of galactosyltransferase was identified as Gal beta 1 leads to 3GalNAc alpha Ser (Thr) by (a) isolation of [14C]Gal-GalNAc-H2 after alkaline borohydride treatment of the 14C-labeled product, (b) establishment of the beta-configuration of the newly synthesized glycosidic bond by its complete cleavage by bovine testicular beta-galactosidase, and (c) assignment of the 1 leads to 3 linkage by identification of threosaminitol obtained from the oxidation of the disaccharide with periodic acid followed by reduction with sodium borohydride, hydrolysis in 4 N HCl, and analysis on an amino acid analyzer. The 1 leads to 3 linkage was confirmed by its resistance to jack bean beta-galactosidase and by the presence of a m/e 307 ion fragment and the absence of a m/e 276 ion by gas-liquid chromatography-mass spectrometry analysis. When acid and beta-galactosidase-treated human tracheobronchial mucin was used as the acceptor, 3.3% of the product was found as [14C]Gal-GalNAc-H2. The remainder of the [14C]Gal was found in longer oligosaccharides formed by a different beta-galactosyltransferase. This galactosyltransferase is slightly inhibited by alpha-lactalbumin and stimulated by spermine.
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PMID:Mucin biosynthesis. Characterization of UDP-galactose: alpha-N-acetylgalactosaminide beta 3 galactosyltransferase from human tracheal epithelium. 680 62

The renal function of workers occupationally exposed to cadmium (n = 148), to mercury vapor (n = 63) or to inorganic lead (n = 25) has been compared with that of workers with no occupational exposure to heavy metals (n = 88). A moderate exposure to lead (Pb-B < 62 microgram/100 ml) does not seem to alter renal function. Excessive exposure to cadmium increases the urinary excretion of both low- and high-molecular-weight proteins and of tubular enzymes. These changes are mainly observed in workers excreting more than 10 microgram Cd/g creatinine or with Cd-B above 1 microgram Cd/100 ml whole blood. Occupational exposure to mercury vapor induces glomerular dysfunction as evidenced by an increased urinary excretion of high-molecular-weight proteins and a slightly increased prevalence of higher beta 2-microglobulin concentration in plasma without concomitant change in urinary beta 2-microglobulin concentration. beta-galactosidase activity in blood and in urine is also increased. The likelihood of these findings is greater in workers with Hg-B and Hg-U exceeding 3 microgram/100 ml whole blood and 50 microgram/g creatinine, respectively. The hypothesis is put forward that the glomerular dysfunction induced by cadmium and mercury might result from an autoimmune mechanism.
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PMID:Assessment of renal function of workers exposed to inorganic lead, calcium or mercury vapor. 744 94

Transformation of NIH3T3 cells with the ras, the sis, or the neu oncogene rendered cells less susceptible to cis-diamminedichloroplatinum(II). Since resistance to cis-diamminedichloroplatinum(II) is reported to be associated with increased levels of metallothionein, we examined effects of these oncogenes on metallothionein gene expression. NIH3T3 cells were first transfected with the lacZ gene whose transcription is under the control of mouse metallothionein I promoter and then with the ras, the sis, or the neu oncogene. The ras and the sis oncogenes increased beta-galactosidase activities which were induced either by metal (cadmium and zinc) or by glucocorticoid (dexamethasone), whereas the neu oncogene repressed its activity. When SV40 early promoter was used instead of metallothionein I promoter for the lacZ gene transcription, the beta-galactosidase activities were not affected by metal, dexamethasone, or any of these oncogenes. This result was coincident with that of reverse transcription polymerase chain reaction that metal-induced MT I mRNA was only detected in the sis- or the ras-transformed cells, whereas any of these oncogenes did not affect the metal-induced transcription of the MT II gene. These results demonstrate that the ras and the sis oncogenes upregulate the metal- or glucocorticoid-induced transcription from metallothionein I promoter, but the neu oncogene negatively regulates it. Thus, resistance to the chemotherapeutic agent by oncogenic transformation is partly associated with the metallothionein gene expression, and MT I and MT II gene expressions are differently controlled by different oncogenes.
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PMID:Effects of oncogenes on the resistance to cis-diamminedichloroplatinum(II) and metallothionein gene expression. 764 18

Elevations in gene dosage of the transcriptional regulatory protein yAP-1 in Saccharomyces cerevisiae can elicit pronounced phenotypic increases in tolerance of a variety of drugs including the toxic heavy metal cadmium. While a large elevation in cadmium tolerance occurs in response to overproduction of yAP-1, the target genes under yAP-1 control have not yet been identified that are responsible for this increase. We show here that the YCF1 gene, encoding a likely integral membrane protein, is required for yAP-1 to exert its normal effects on cadmium tolerance. Mutant strains of yeast that lack the YCF1 gene are hypersensitive to cadmium and this hypersensitivity is epistatic to yAP-1 overexpression. YCF1 mRNA levels and the expression of a YCF1-lacZ reporter construct positively correlates with changes in YAP1 gene dosage. A set of 5' truncation derivatives of the YCF1-lacZ fusion gene identified the region from -201 to +47 as being sufficient for the yAP-1-dependent increase in expression. DNase I footprinting using a probe from this segment of the YCF1 promoter showed that bacterially-produced yAP-1 protein was capable of binding a novel DNA element we have designated the yAP-1 response element. Insertion of the yAP-1 response element upstream of a CYC1-lacZ gene fusion led to the production of beta-galactosidase in a yAP-1-dependent fashion. These data establish that an important physiological target of yAP-1 transcriptional regulation is the YCF1 structural gene.
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PMID:Cadmium tolerance mediated by the yeast AP-1 protein requires the presence of an ATP-binding cassette transporter-encoding gene, YCF1. 779 63

A corticotropin-releasing hormone (CRH) and cAMP-responsive region (-236/-133) in the rat POMC gene promoter previously reported to confer CRH/cAMP responsiveness to heterologous reporter constructs has been characterized. DNAse footprint analysis revealed that multiple elements in this region were bound by nuclear proteins from the POMC expressing AtT20 cells. When these individual DNA elements were separately tested in heterologous reporter constructs for CRH induction, only one element, designated PCRH-RE (POMC CRH responsive element, -171/-160) was found to give strong CRH stimulation (5- to 7-fold). This element appears novel as to the possible binding factors, although it has homology to the mouse metallothionein metal regulatory element. Gel shift analyses of the PCRH-RE with AtT20 cell nuclear extracts showed marked stimulation of retarded nucleoproteins following CRH stimulation, suggesting that the possible binding factor(s) may mediate transcriptional regulation at this site. The activity of PCRH-RE binding protein was inhibited by divalent cations, with Cu2+ and Cd2+ being most effective; Zn2+ had no effect, indicating that this binding factor(s) is functionally distinct from the metallothionein metal regulatory element binding protein. A 2.6 kilobase cDNA clone encoding a protein (PCRH-REB-1) binding to this element was isolated by Southwestern screening of an AtT20 expression library with radiolabeled PCRH-RE oligonucleotides. This clone was used to isolate several other cDNA clones to determine the sequence corresponding to the entire coding region of the protein (PCRH-REB), which proved to be identical to a recently described DNA binding protein of the replication factor C complex, mRFC140/Mouse Southwestern. Primer extension and Northern blot analysis revealed that the size of the full length mRNA is about 4.9 kilobases. PCRH-REB mRNA expression is not restricted to corticotrophs but is present in a broad tissue distribution as evaluated by reverse transcription polymerase chain reaction analysis. A bacterially expressed beta-galactosidase-PCRH-REB-1 fusion protein was shown to bind PCRH-RE efficiently. Furthermore, binding of the PCRH-REB-1 fusion protein to the POMC CRH-responsive element was inhibited by divalent cations with similar sensitivities to those observed using AtT20 nuclear extracts. The predicted PCHR-REB protein sequence presents several interesting motifs: one p-Loop motif (ATP binding site), nine protein kinase A phosphorylation sites (implying a possible role in responding to the CRH-induced cAMP signal), and regions of homology to proteins involved in DNA replication and repair. PCRH-REB is, therefore, a potential transacting factor binding to a major CRH-responsive element in the POMC promoter.
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PMID:Characterization of a corticotropin-releasing hormone-responsive element in the rat proopiomelanocortin gene promoter and molecular cloning of its binding protein. 785 55

Two genes (mtl-1 and mtl-2) that encode the novel metallothioneins (MTs) of Caenorhabditis elegans (CeMTs) were cloned and characterized. Both genes contain a single intron that interrupts codon 6 and short 3'-untranslated regions. However, their promotor regions are distinctively non-homologous. The mtl-2 promoter contains a TATAA box and a single putative metal regulatory element. These elements are absent in the mtl-1 promoter. Nevertheless, both CeMT1 and CeMT2 mRNAs are induced by cadmium and contain precisely initiated, 5'-untranslated sequences. The inducibility and cell type specificity of metallothionein gene expression were investigated in transgenic C. elegans that carry the lacZ (beta-galactosidase) reporter gene under the control of an mtl-1 or mtl-2 promoter sequence. Upon treatment of transgenic C. elegans with cadmium or heat stress, the mtl-2:lacZ fusion gene is abundantly and exclusively expressed in the intestinal cells of larvae and adult animals. Expression is not detected in the absence of metal or heat shock. In contrast, an mtl-1:lacZ construct is constitutively expressed in the pharynx and induced by cadmium and heat shock in the intestinal cells of C. elegans larvae. The metal-inducible expression of the mtl-1:lacZ gene is attenuated in adult transgenic nematodes. Thus, the activity of each mtl promoter is modulated by metals as well as developmental and environmental factors.
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PMID:The novel metallothionein genes of Caenorhabditis elegans. Structural organization and inducible, cell-specific expression. 842 32

Inhibition by ethanol of the activities of lysosomal exoglycosidases in stomach, small intestine, liver and brain of rats exposed to cadmium (Cd2+) was determined. Out of the glycosidases tested the most distinct effect of Cd2+ and ethanol administered to the rats in vivo was observed in the small intestinal mucosa in a decreasing order: N-acetyl-beta-hexosaminidase, beta-galactosidase and alpha-fucosidase.
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PMID:Influence of ethanol on the activity of glycosidases in rats exposed to cadmium (Cd2+). 858 79


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