Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using electrophysiological techniques we have examined the apical membrane ionic permeabilities of primary cell cultures of the mouse mammary gland in the midpregnant, preneoplastic, and neoplastic states. Membrane Na+ permeability changed with tumorigenesis, whereas K+ and Cl- permeabilities were unaltered. With tracer flux techniques the unidirectional efflux rate constant of 22Na was found to be greater in tumor cells than it is in normal cells. This increase in 22Na efflux was eliminated by the addition of ouabain. The results are interpreted as an increase in Na+ permeability and in Na+-K+-ATPase activity with the neoplastic transformation. The presence or absence of the virus in midpregnant cells does not seem to affect Na+ permeability.
Cancer Res 1978 May
PMID:Alteration of sodium transport in mouse mammary epithelium associated with neoplastic transformation. 20 64

Susceptibility of human skin fibroblasts to SV40 virus infection has been suggested as a marker of cancer risk. To evaluate the role of heritable factors in the regulation of SV40 T-antigen, fibroblasts from 9 pairs of identical twins and 129 members of cancer-prone families, including 16 with cancer, were tested in a 3-day immunofluorescence assay. In the twin study, the variance of T-antigen values was significantly less in identical than in fraternal or non-twin sibs, suggesting a heritable component in the regulation of SV40 infection. In the families, T-antigen values of parents and children were compared to models of Mendelian inheritance. At least three modes of inheritance--autosomal dominant, recessive, and X-linker--were observed. The distribution of offspring values compared to those of their parents suggested that interaction of multiple genetic factors influences the T-antigen value in individual patients. With the exception of Fanconi's anemia, the values for patients with cancer or predisposing syndromes were not uniformly elevated. The utility of this assay as a marker of cancer risk appears limited because of the complexity of factors that influence T-antigen expression in individual cases.
Int J Cancer 1978 Sep 15
PMID:Genetics of SV40 T-antigen expression: studies of twins, heritable syndromes and cancer families. 21 68

The antitumor antibiotic Adriamycin is a potent inhibitor of the sodium-potassium-activated adenosine triphosphatase of native heart microsomes. Adriamycin also inhibits potassium transport (although not sodium transport) in slices of kidney cortex. The effects on both the adenosine triphosphatase and ion transport are markedly reduced by Ca2+, probably by chelation of this metal by Adriamycin. These effects could provide a basis for explaining the Adriamycin cardiotoxicity as a digitalis-type toxicity.
Cancer Res 1979 Jan
PMID:Inhibition of sodium-potassium-activated adenosine 5'-triphosphatase and ion transport by adriamycin. 21 83

The ATPase inhibitor quercetin, which inhibits tumor glycolysis, was shown to be a glucose transport inhibitor like the chemically related compound phloretin. Rat thymocyte glucose transport stimulated by the mitogens concanavalin A or ionophore A 23187 was more sensitive than unstimulated transport to quercetin inhibition. The partial inhibition of Na+-, K+- ATPase activity by quercetin observed in tumor cells was confirmed in thymocyte plasma membranes. The specific Na+-, K+- ATPase inhibitor ouabain did not mimic the effect of quercetin on mitogen-stimulated glucose transport but did reduce the effectiveness of concanavalin A as a stimulator of mitochondrial pyruvate oxidation. The results support the idea that glycolytic flux and the activity of plasma membrane ATPase are related but suggest that glucose transport, rather than the Na+-, K+-ATPase, is the rate-limiting reaction in lymphocytes.
J Natl Cancer Inst 1979 May
PMID:Preferential inhibition by quercetin of mitogen-stimulated thymocyte glucose transport. 22 Apr 48

Sarcomas were induced in CFW mice by the iv inoculation of simian virus 40 (SV40) in neonatal animals. Infection with murine malaria parasites, Plasmodium berghei yoelli, decreased the latency and increased the incidence and invasiveness of the tumors. All mice given both SV40 and P. berghei yoelli had sarcomas of the liver and spleen at 9 months of age. At 11 months of age, 70% of the SV40-inoculated mice had sarcomas of the liver indistinguishable from those in the group given both pathogens. Only 1 lung metastasis was seen in the SV40-treated group. The sarcomas contained SV40 T-antigen as revealed by the indirect immunofluorescence technique. Among adult CFW mice given iv injections of SV40, only 2 tumors were found at 11 or 12 months after virus inoculation. Both tumors were in the lungs; 1 was an adenoma and 1 was a papillary adenocarcinoma. Neither gave a positive reaction with the immunofluorescence test.
J Natl Cancer Inst 1979 Oct
PMID:Sarcomas induced by injection of simian virus 40 into neonatal CFW mice. 22 3

The molecular mechanisms involved in the inactivation of (Na+ + K+)-stimulated ATPase of Yoshida sarcoma cells by a cytotoxic protein (P6) from cobra venom have been examined. The overall data obtained using purified (Na+ + K+)-stimulated ATPase of Yoshida sarcoma cells suggest that cytotoxin P6 combines with phosphatidyl serine and a glycolipid which are closely associated with (Na+ + K+)-stimulated ATPase which in turn may lead to the inactivation of the enzyme in this cell system.
Cancer Biochem Biophys 1979
PMID:Inactivation of membrane-bound (Na+ +K+)-ATPase of Yoshida sarcoma cells and cobra venom cytotoxin complex with the glycolipid components of the enzyme system. 22 83

Inactivation of (Na+ + K+)-ATPase of Yoshida sarcoma cells and beef brain microsomes by phospholipase A2 and a cytotoxin P6 from snake venom has been examined in relation to their activity to degrade phospholipids. Cytotoxin P6 which was most basic and devoid of phospholipase activity was most effective in inhibiting the (Na+ + K+)-ATPase of Yoshida sarcoma cells. Phospholipase A2 from Naja naja which was most active in degrading phospholipids was least effective in inhibiting (Na+ + K+)-ATPase in Yoshida sarcoma cells or in beef brain microsomes. Addition of trace amounts of cytotoxin P6 to the phospholipase considerably enhanced the inactivation of (Na+ + K+)-ATPase. The evidence suggests that the charge of the inhibitor protein and its specific structure play an important role in the inactivation of (Na+ + K+)-ATPase.
Cancer Biochem Biophys 1979
PMID:Influence of charge on the inactivation of membrane bound (Na+ + K+)-ATPase of Yoshida sarcoma cells by inhibitor proteins from cobra venom. 23 2

Continuous epithelial-like cell lines derived from normal adult rat liver and hepatocarcinomas were evaluated for their growth in soft agar and five properties of the cell membrane as markers for neoplastic transformation. A correlation of these properties was made to the tumorigenicity of the lines in nude mice. Growth in soft agar was a specific and sensitive marker, whereas the data on uptake of 2-deoxy-D-glucose were consistent, with high uptake being a specific but clearly not a sensitive marker. Agglutination and hemadsorption mediated by concanavalin A, multinucleation in the presence of cytochalasin B, and the cell membrane activity of adenosine triphosphatase did not correlate with tumorigenicity of the other markers for transformation. In addition, it is shown that Mycoplasma infection does not alter any of these properties but that infection can be eliminated by passage of cells through nude mice.
Cancer Res 1979 Mar
PMID:A survey of growth in soft agar and cell surface properties as markers for transformation in adult rat liver epithelial-like cell cultures. 42 43

Limitless numbers of various genetic structures have been formed in chromosomes and plasmids and numerous bioactive compounds are produced by microorganisms. Therefore, it may be said that compounds useful in treatment of cancer will be found more and more in microbial secondary metabolites and more effective antitumor antibiotics and their derivatives, or more effective products producing immune resistance to cancer, will be discovered. In these studies, as discussed in this paper, the most urgent problem is to establish a rational screening principle or system to select compounds worth clinical examination. This is particularly important in the analog area. Bleomycin is an analog of phleomycin chosen because of lower renal toxicity. It has become an antitumor agent of significant value. Macromycin is a new structure which has been found to bind with animal cells and inhibit growth. Neothramycin is a new benzodiazepine antibiotic which has lower toxicity than other structures studied in this class and is active against L1210, Yoshida sarcoma, and Sarcoma 180. Aclacinomycin A is an analog of adriamycin chosen for clinical study based on its low cardiac toxicity and high distribution in mouse lung and spleen. Coriolins are another new structural class. Diketocoriolin B has activity in L1210 leukemia and has been shown to inhibit Na-K-ATPase. Bestatin is a compound which inhibits aminopeptidase B and leucine aminopeptidase has been shown to increase delayed hypersensitivity. Bestatin also increases the effects of other antitumor agents such as adriamycin, and bleomycin.
Recent Results Cancer Res 1978
PMID:New microbial secondary metabolites under preclinical development for cancer treatment. 70 7

A magnesium-independent deoxyuridine-5'-triphosphatase was found in Yoshida sarcoma cells but not in normal rat liver. The phosphatase is specific for deoxyuridine 5'-diphosphate and deoxyuridine triphosphate, and its Km for deoxyuridine triphosphate is 2.7 X 10(-7) M. The enzyme was not inhibited by fluoride and required no divalent cations. Thus it differs from known nucleotide phosphatases. Deoxyuridine monophosphokinase, which is detectable in a crude extract of normal rat liver, could not be detected in an extract of Yoshida sarcoma cells. However, with hydroxylapatite column chromatography of the extract, a deoxyuridine 5'-monophosphate kinase activity as high as that in normal rat liver was found in fractions separated from the phosphatase activity. Thus the absence of detectable deoxyuridine 5'-monophosphate kinase activity in the crude extract of Yoshida sarcoma cells is due to the presence of this nucleotide phosphatase.
Cancer Res 1977 Jun
PMID:A new deoxyuridine-5'-triphosphatase in Yoshida sarcoma cells involved in deoxyuridine 5'-triphosphate metabolism. 85 39


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