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:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate further the pathophysiology of rotavirus-induced diarrhea, changes in specific activities of eight relevant intestinal enzymes [alkaline phosphatase, thymidine kinase, lactase, maltase, sucrase, Na+,K+-adenosine triphosphatase (ATPase), adenylate and guanylate cyclases] were measured following infection of suckling mice with murine rotavirus (epizootic diarrhea of infant mouse strain) and compared with age-matched control mice. The concentration of lactose within the lumen of the gastrointestinal tract during infection was also measured. During the course of infection, activities of alkaline phosphatase and lactase decreased, whilst the activity of thymidine kinase increased. Precocious maturation profiles of sucrase and maltase enzymes were observed. No significant changes were detected in the activities of Na+,K+-ATPase or the adenylate and guanylate cyclases. These results are discussed in relation to existing and novel hypotheses on the pathogenesis of rotavirus-induced diarrhea.
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PMID:Intestinal enzyme profiles in normal and rotavirus-infected mice. 289 74

We have demonstrated that X-rays induce mutations at 4 of 5 genetic loci. 2 of these loci, which code for a mRNA synthesis factor (resistance to 5,6-dichlororibofuranosylbenzimidazole) and tubulin (resistance to podophyllotoxin), are "small-marker" loci, in that they theoretically respond only to mutations which eliminate a toxin-binding site while leaving the major function of the protein intact. Thus mutations induced by X-rays in these two loci are most likely due to base-pair substitution-type alterations. X-Rays did not induce mutations in the Na+/K+ ATPase (resistance to ouabain), another small-marker locus. Two other loci, hypoxanthine guanine phosphoribosyl transferase (resistance to 6-thioguanine) and thymidine kinase (resistance to trifluorothymidine), are "whole-gene" targets in that they theoretically respond to a wide variety of mutagenic changes. X-Rays induced dose-dependent increases in mutant fraction at both of these loci. Ethyl methanesulfonate (EMS), an agent thought to produce mutations primarily through a base-pair substitution mechanism, induced mutations at all genetic loci tested. The pattern of mutations at the small-marker loci induced by EMS was different than that induced by X-rays, suggesting that the specificities of the mutagens and/or of the loci are different.
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PMID:X-rays mutate human lymphoblast cells at genetic loci that should respond only to point mutagens. 301 57

We measured the response of jejunal sodium (Na) absorption to neutral amino acid (L-alanine) and to dipeptides (L-alanyl-L-alanine, glycylsarcosine) in normal piglets and in piglets with acute viral diarrhea after experimental infection with transmissible gastroenteritis (TGE) virus. In the TGE jejunum villi were blunted, crypts were deepened, and the epithelium was composed of relatively undifferentiated cells with reduced disaccharidase, decreased sodium-potassium-stimulated ATPase, and elevated thymidine kinase activities. The response of Na absorption to a maximal concentration of L-alanine (20 mM) or D-glucose (30 mM) was significantly blunted in TGE jejunum in Ussing chambers. However, the addition of L-alanine together with D-glucose caused a significantly greater increment of Na absorption than either L-alanine or D-glucose alone in control and TGE tissue. The effect of Na absorption of the dipeptide L-alanyl-L-alanine (10 mM), which was rapidly hydrolyzed by control and TGE mucosa, was similar to that of L-alanine (20 mM), while glycylsarcosine, a poorly hydrolyzed dipeptide, did not change net Na absorption in the jejunum. Our data support the concept of separate carrier systems for neutral amino acid and hexose in the crypt-type intestinal epithelium characterizing viral enteritis. We speculate that a sodium-cotransporting amino acid, if added to oral glucose-electrolyte solutions, could benefit oral rehydration therapy in acute viral diarrhea; neither of the dipeptides tested here can be expected to enhance absorption to any greater extent than its constituent amino acids.
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PMID:Alanine enhances jejunal sodium absorption in the presence of glucose: studies in piglet viral diarrhea. 301 59

In the relatively undifferentiated jejunal mucosa occurring in piglet viral enteritis, we measured the response of transepithelial Na+ and Cl- fluxes in vitro to raised intracellular adenosine 3',5'-cyclic monophosphate (cAMP) levels. At the acute 40-h stage of transmissible gastroenteritis (TGE), luminal membrane markers, sucrase and lactase, and a basolateral jejunal epithelial membrane marker Na+-K+-ATPase, were significantly decreased in activity, while a proliferative marker, thymidine kinase, was significantly enriched; these enzyme characteristics are typical of enterocytes isolated from crypts of other species. As expected, control piglet jejunum in short-circuited Ussing chambers after theophylline (10 mM) developed significant net secretory Na and Cl fluxes primarily due to significant antiabsorptive effects (delta JNa m----s = 3.48 +/- 0.52, delta JCl m----s = 2.59 +/- 0.28). Furosemide (10(-4) M), an inhibitor of electroneutral NaCl cotransport, produced antiabsorptive effects (delta JNa m----s = 2.53 +/- 0.31, delta JCl m----s = 2.58 +/- 0.28) in control jejunum that were not significantly different from those seen in response to theophylline. TGE jejunum, however, responded to theophylline not by an antiabsorptive effect but by significant electrogenic Cl- secretion (delta JCl s----m = 1.59 +/- 0.48); furosemide had no effect on ion fluxes in TGE tissue. Control and TGE jejunal mucosal homogenates did not differ in their basal or theophylline-stimulated levels of cAMP. We conclude that the relatively undifferentiated small intestine occurring in acute TGE does not generate either a cAMP-mediated antiabsorptive effect or a furosemide-mediated antiabsorptive effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Absence of a cAMP-mediated antiabsorptive effect in an undifferentiated jejunal epithelium. 303 40

The mutagenic effect of cadmium chloride on somatic cells of F1 hybrid mice CBA X C57B1/6J in vivo and on an established line of CHO-ATZ-2 Chinese hamster cells in vitro has been studied. The induction of micronuclei has been demonstrated in mouse marrow cells as well as induction of point mutations at loci controlling the synthesis of hypoxanthine-phosphoribosyltransferase, thymidine kinase, adenine phosphoribosyltransferase and the resistance of Na+/K+ ATPase to ouabain in the cell line CHO-AT-2. A peak of mutagenic activity under the action of subtoxic doses of cadmium chloride has been revealed.
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PMID:[Mutagenic action of cadmium chloride in mammals]. 343 31

To investigate the effect of chronic protein-calorie malnutrition on intestinal repair after an enteric infection, we examined small intestinal structure, enzyme activity, and sodium transport in undernourished piglets during the acute and convalescent phases of a viral enteritis, transmissible gastroenteritis (TGE). Gnotobiotic pigs, nutritionally deprived from the age of 7 days, gained less weight than dietary controls from 14 days of age until the end of the study. Animals from malnourished and control diet groups were inoculated with TGE virus at 22-23 days and studied during the acute (40 h) and convalescent (4, 10, and 15 days) stages of this experimental enteritis along with noninfected dietary controls. After TGE infection, we observed a further decrease in weight gain and an increased mortality only in undernourished pigs. In jejunum and ileum of both dietary groups at 40 h after TGE infection, we observed comparable structural lesions, similar decreased activities of mucosal enzymes (sucrase, lactase, sodium-potassium-dependent ATPase), and increased thymidine kinase activities. Also we noted comparable diminution of glucose-stimulated jejunal sodium absorption in both dietary groups at 40 h. In control diet pigs, transport abnormalities recovered by 4 days after TGE infection and normal mucosal structure and enzyme activity returned over 4-15 days. In undernourished piglets, structural repair and enzyme abnormalities were prolonged when compared with the control diet group; glucose-stimulated sodium transport did not recover until 10 days after infection and never regained the enhanced activity seen in noninfected undernourished controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impact of chronic protein-calorie malnutrition on small intestinal repair after acute viral enteritis: a study in gnotobiotic piglets. 392 24

Hybrid cell clones between mouse cells deficient in thymidine kinase (EC 2.7.1.21) and two different human cell lines transformed by simian virus 40 (SV40) and deficient in hypoxanthine phosphoribosyltransferase (EC 2.4.2.8) were examined for SV40 tumor (T) antigen(s). Concordant segregation of the gene(s) for SV40 T antigen and human chromosome C-7 was observed in these hybrids. The human chromosome C-7 which contains the gene(s) for SV40 T antigen is preferentially retained by the majority of the hybrid clones tested. When hybrid clones positive and negative for SV40 T antigen, derived from the fusion of SV40-transformed Lesch-Nyhan fibroblasts with mouse cells, were fused with CV-1 permissive cells, SV40-specific V antigen was observed only in the cultures derived from fusion of the hybrid clones positive for T antigen. This result indicates a linkage relationship between human chromosome C-7, SV40 T-antigen gene(s), and SV40 genome(s) integrated in the human transformed cells.
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PMID:Assignment of the T-antigen gene of simian virus 40 to human chromosome C-7. 435 83

Thymidine kinase-negative Friend leukemia cells were cotransfected with simian virus 40 (SV40) DNA and thymidine kinase gene DNA of herpes simplex virus type 1. The transfected thymidine kinase-positive cells were selected in HAT medium, and SV40 T-antigen expression was observed over many months in cells cultured under selective conditions, and after adaptation to normal growth medium under nonselective conditions. It was shown by Southern blot hybridization that SV40 DNA was integrated in multiple copies in the chromosomal DNA of several clones. All SV40 DNA-containing Friend leukemia cell clones analyzed were able to undergo induced erythroid differentiation. Induced cultures still expressed SV40 T-antigen to the same extent that untreated control cultures did.
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PMID:DNA-mediated gene transfer in Friend leukemia cells by cotransfection of simian virus 40 DNA with herpes simplex virus thymidine kinase DNA. 629 44

The nucleotide sequence of a 2549-bp DNA fragment containing the entire coding region of the marmoset herpesvirus (MarHV) thymidine kinase gene (tk) and the flanking sequences was determined by the dideoxynucleotide chain termination method. The MarHV thymidine kinase polypeptide predicted from the nucleotide sequence contained 376 amino acids and had a molecular weight of 41,281. The sequencing data also reveal that the coding portion of another MarHV gene probably begins only 292 nucleotides downstream from the stop codon of the MarHV tk gene. There was relatively little nucleotide sequence homology between the MarHV tk gene and that of the herpes simplex virus (HSV) types 1 and 2 tk genes. Comparisons of the predicted amino acid sequences of the MarHV thymidine kinase polypeptide with that of the HSV-1 and HSV-2 thymidine kinase polypeptides, however, revealed clear, but interrupted, homology within several regions of the polypeptide chains. Amino acid sequence homology was particularly striking at residues 10 to 27 of the MarHV thymidine kinase polypeptide and residues 49 to 66 of the HSV-1 and HSV-2 thymidine kinase polypeptides. These same amino acid residues exhibit noticeable sequence homology to the mitochondrial beta subunit ATPase, oncogene p21 protein, adenylate kinase, and to other nucleotide-binding proteins. It has been proposed that the indicated regions of homology are elements of a nucleotide-binding pocket in ATPase, p21, and adenylate kinase, raising the possibility that amino acid residues 15 to 25 of the MarHV thymidine kinase and 54 to 64 of the HSV-1 and HSV-2 enzymes are likewise parts of nucleotide-binding sites.
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PMID:Nucleotide sequence of the marmoset herpesvirus thymidine kinase gene and predicted amino acid sequence of thymidine kinase polypeptide. 633 Sep 76

Chemical mutagenesis in animal cells is a complex process. Whereas some chemicals are mutagenic in their original form, others such as the nitrosamines and polycyclic hydrocarbon carcinogens are mutagenic only when enzymatically activated. The active form, or ultimate carcinogen, can interact with proteins and nucleic acids, altering amino acids and producing modified bases in DNA. The modified bases do not usually constitute mutations as produced. Instead they are acted on by the DNA enzymes of the cell, which repair most damaged bases but occasionally insert incorrect base sequences at or near the sites of damage. The frequency at which mutant animal cells are recovered depends upon the selection conditions in culture, upon whether the mutation selected is in a gene present in single or multiple active copies, and upon whether expression is dominant or recessive. Many studies depend on selecting for 8-azaguanine- or 6-thioguanine-resistant mutants, which are due to mutations in the HGPRT locus present in a single active copy on the X-chromosome. Other widely used systems depend on selecting for ouabain resistance, which is dominant and results from a change in the sodium/potassium ATPase activity, or on selecting for thymidine kinase mutants in heterozygous Tk+/Tk- mouse cells. Many other types of mutation including nutritional markers are recessive and express only in cells carrying a single active gene copy, as is sometimes the case in established cell lines. The types of base damage causing mutations have been identified in very few cases only, and little is known about the enzymatic mechanisms of mutagenesis. However, chemical mutagenesis in cultured animal cells provide a practical way of testing chemicals and radiations for mutagenicity directly in animal cells, and much has been learned about the mutagenicity of various carcinogenic substances. To date, there is reasonable qualitative agreement between these results and those obtained in the widely used liver microsome-activated bacterial mutagenesis test systems.
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PMID:International Commission for Protection against Environmental Mutagens and Carcinogens. ICPEMC working paper 2/5: mutagenesis in mammalian cells. 702 63


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