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

---

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

Ultrastructural, enzyme histochemical (acide phosphatase, adenosine triphosphatase, neutral 5'-nucleotidase) and immunohistochemical (cytokeratins with monoclonal antibodies BH11 and BC3) features of the thymus cortical epithelial cells of leukemic DBA/2 inbred mice have been studied. In the leukemic mice epithelial cells appeared possessing some ultrastructural and histochemical features of cell activation. Lympho-epithelial complexes, composed mainly of BH11 and BC3 immunoreactive cells and of lymphoid cells were subcapsulary and subseptally found. It is discussed on the eventual involvement of the lympho-epithelial complexes in the intrathymic leukemogenesis during lymphoid leukemia.
...
PMID:Structural and histochemical features of cortical thymic epithelial cells in mice with chemically-induced lymphoid leukemia. 324 59

The plasma membrane of the mouse peritoneal macrophage has specific receptors which enable the cell to bind IgG or complement-coated sheep red cells and is also rich in a divalent cation-dependent adenosine triphosphatase (ATPase) activity. L cells lack these macrophage membrane markers. The question of macrophage membrane receptor expression was investigated in DBA/2 mouse macrophage x mouse LMTK(-) cell hybrids produced with the aid of Sendai virus. Three independent clones and one mass culture were isolated by their ability to grow in hypoxanthine, aminopterin, and thymidine (HAT) selection medium. These hybrids retained 85-100% of the sum of two parent cells' chromosomes and expressed several genes derived from both parents, including glucose phosphate isomerase isozymes and H-2 antigens. The hybrids displayed ATPase activity which was intermediate between that of the macrophage and L cell. The macrophage specific receptors for antibody or complement-coated red cells could not be demonstrated on hybrid cells. The selective absence of these receptors is probably because of a failure in gene expression rather than to loss of genes.
...
PMID:The preparation and properties of macrophage-L cell hybrids. 432 56

Total, Mg2+, and Na+, K+ ATPase activities were studied in fresh brain homogenates of the audiogenic seizure (AGS)-resistant C57BL/6J (B6) and AGS-susceptible DBA/2J (D2) inbred strains and in 13 B6 X D2 (BXD) recombinant inbred (RI) strains. These activities were also studied in the D2.B6-Iasb congenic mice, that are similar genetically to D2 mice, except for the Iasb gene which inhibits the spread of AGS activity. The total and Mg2+ ATPase activities of the brainstem were significantly lower in the D2 than in the B6 mice at 21 days of age. No differences were found between these strains for Na+,K+ ATPase activity. The total, Mg2+, and Na+,K+ ATPase activities in the B6 brainstem did not change noticeably from 21 to 80 days of age. In the D2 brainstem, however, the Mg2+ activity increased with age, and the Na+,K+ ATPase activity decreased from 30 to 80 days of age. No genetic associations could be found between AGS susceptibility and total or Mg2+ ATPase activities in the D2.B6-Iasb mice or among the 13 BXD RI strains. Hence, differences in genetic background, rather than differences in AGS susceptibility, can account for the lower ATPase activities in 21-day-old D2 mice. Further, the Mg2+ and Na+,K+ ATPase activities appear to be regulated by more than one gene. This study emphasizes the utility of RI and congenic strains for testing the biochemical basis of AGS susceptibility in mice.
...
PMID:Genetic study of cationic ATPase activities and audiogenic seizure susceptibility in recombinant inbred and congenic strains of mice. 614 Dec 22

DBA/2J mice are susceptible to audiogenic seizures (ASs) in an age-dependent manner, susceptibility being maximal at 21 days of age and declining thereafter. DBA, as compared with AS-resistant C57BL/6J (C57) mice, had higher carbonic anhydrase (CA) activity in cerebral cortex, brainstem, and cerebellum homogenates at 21 days of age. CA activity was also increased in cytosolic (82%), microsomal (167%), and myelin (68%) subcellular fractions from cerebral cortex, and in cytosolic (51%) and mitochondrial (102%) fractions from brainstem of DBA mice at 21 days of age. In addition, DBA mice had a higher Na+, K+-ATPase activity in myelin from cerebral cortex, and a lower HCO3--ATPase activity in mitochondria from brainstem. The differences in CA activity in the cerebral cortex and in HCO3--ATPase were not present at 110 days of age, when DBA mice are no longer susceptible to ASs. Because CA and HCO3--ATPase are involved in maintaining a proper ionic environment for neuronal function, these data suggest that alterations in activity of these enzymes are related to the age-dependent changes in AS susceptibility in DBA mice.
...
PMID:Subcellular distribution of carbonic anhydrase and Na+, K+- and HCO3--ATPases in brains of DBA and C57 mice. 623 73

The prevalence and severity of polycystic kidney disease (PKD) induced by glucocorticoids in mice can be predicted by a mathematical "threshold" model. We studied the relationship between Na-K ATPase activity and cyst formation in C3H (low threshold for PKD) and DBA mice (high threshold). There was no difference in Na-K ATPase induction by 200 mg/kg methyl prednisolone acetate (MPA) (C3H; 97.4 nmol NADH/min/mg protein: DBA; 94.2 nmol NADH/min/mg protein). C3H mice demonstrated greater cyst formation than DBA animals as measured by area (20.1% relative area vs 13.9%, p < 0.05) or by calculated volume (7.4% relative volume vs 2.3%, p < 0.001). Significant relationships were seen between Na-K ATPase activity and logarithmically transformed area data in C3H animals and with cyst volume in both strains. Na-K ATPase activity is related to cyst formation in glucocorticoid induced PKD, but the level of Na-K ATPase activity is not a determinant of the threshold for glucocorticoid induced PKD.
...
PMID:Na-K ATPase activity in murine glucocorticoid induced polycystic kidney disease in vivo. 768 65

Recently, it has been reported that Na,K-ATPase in the renal epithelia of human autosomal dominant polycystic kidney disease and cpk mouse, a murine model of autosomal recessive polycystic kidney disease, mislocates to apical plasma membrane and that mislocated Na,K-ATPase causes the cyst formation. Whether the DBA/2FG-pcy mice, which are presumably a suitable model for autosomal dominant polycystic kidney disease, also exhibit the reversal polarity of Na,K-ATPase localization was examined. Kidneys of newborn DBA/2FG-pcy mice, and those at early and late stages of cyst development were examined by immunohistochemical techniques. At any stage, abnormal distribution of Na,K-ATPase on the apical membranes of tubular epithelial cells could not be detected. It is suggested that cysts can be formed without reversed polarity of Na,K-ATPase distribution in pcy mice.
...
PMID:Sodium pump distribution is not reversed in the DBA/2FG-pcy, polycystic kidney disease model mouse. 791 57

A Ca(2+)- or Mg(2+)-stimulated ecto-ATPase is thought to regulate the hydrolysis of extracellular ATP in nervous tissues. The hydrolysis of nucleotide triphosphates (NTPs) was analyzed in brain microsomal fractions from crosses of DBA/2J (D2) and C57BL/6J (B6) mice. The nucleotide triphosphatase (NTPase) activity was significantly reduced in D2 mice as compared to B6 mice, and B6D2F1 hybrids had activities intermediate to the parentals. A significant positive correlation was found between the hydrolysis of four NTPs (ATP, CTP, GTP and UTP) in 24 B6 x D2 (BXD) recombinant inbred (RI) strains of mice and in 80 B6D2F1 x D2 backcross mice. The RI strains and backcross mice fell into two distinct groups with respect to the NTPase activity. Linkage of NTPase activity was suggested with the chromosome 2 markers, D2Mit6 and Ass-1, in the RI strains, and was confirmed by analysis of other markers in the backcross population. These data suggest that the Ca(2+)- or Mg(2+)-stimulated hydrolysis of NTPs, designated Ntp, is regulated by a single gene located on proximal chromosome 2. Although an association was observed previously between Ca(2+)-ATPase activity and susceptibility to audiogenic seizures (AGS), no significant association was observed for the expression of Ntp and AGS susceptibility.
...
PMID:Genetic analysis of nucleotide triphosphatase activity in the mouse brain. 805 15

Effects of chronic treatment of dibutyryl cyclic AMP (db-cyclic AMP) on Na+,K(+)-ATPase activity in cell homogenates and intracellular Na+ and K+ contents [(Na+)i and (K+)i] were studied in primary cultures of astrocytes derived from cerebral cortex of neonatal audiogenic seizure-susceptible DBA and audiogenic seizure-resistant C57 mice. Na+,K(+)-ATPase activity in cell homogenates was greater and (Na+)i was less in DBA astrocytes than in C57 astrocytes. There was no difference in (K+)i between astrocytes from DBA and C57 mice. Addition of db-cyclic AMP to the medium from day 14 to day 21 in culture (final concentration 0.25 mM) increased Na+,K(+)-ATPase activity in cell homogenates and decreased (Na+)i, but had no significant effect on (K+)i in astrocytes from either DBA or C57 mice. Chronic treatment with db-cyclic AMP altered cell growth. Protein and DNA content of cultured astrocytes from both DBA and C57 mice was decreased. DNA was more affected than protein. Modifying K+ and Na+ concentration in medium altered Na+,K(+)-ATPase activity in cell homogenates as well as (Na+)i and (K+)i in cultured astrocytes of both DBA and C57 mice. Changes in (Na+)i and (K+)i at different K+ concentrations in medium paralleled those in Na+,K(+)-ATPase activity in cell homogenates. Results indicate that the ability to transport Na+ across the cell membrane and the response of Na+,K(+)-ATPase to db-cyclic AMP and to the changes in K+ in medium of cultured astrocytes from audiogenic seizure-susceptible DBA mice are sufficient.
...
PMID:Effects of dibutyryl cyclic AMP on Na+,K(+)-ATPase activity and intracellular Na+ and K+ in primary cultures of astrocytes from DBA and C57 mice. 811 47

Cyst formation in polycystic kidney disease (PKD) involves proliferation of cyst lining epithelial and changes in trans-epithelial fluid and electrolyte transport. In vitro studies have suggested that mislocation of Na,K-ATPase to the apical tubular surface may be an important component of cyst fluid transport. We undertook in vivo studies of Na,K-ATPase location using the "threshold" murine model of glucocorticoid-induced PKD (GIPKD). Using histological, immunohistochemical, and densitometric techniques, we compared cyst formation and the cellular location of Na,K-ATPase in suckling C3H (low threshold for GIPKD) and DBA (high threshold) mice given an inducing dose of 200 mg/kg methylprednisolone acetate. As expected, C3H mice demonstrated greater cyst formation as measured by proportion of section area occupied by the tubule lumen (26.7% vs 15.5%; p < 0.001). Cyst formation was associated with increased Na,K-ATPase staining and increased apical Na,K-ATPase location. MPA treatment in C3H mice resulted in apical staining that exceeded basolateral staining (35.3% of reference window vs 29.8%; p < 0.001). The relatively GIPKD-resistant DBA mice did not show such change in Na,K-ATPase location. These immunohistochemical studies suggest a role for Na,K-ATPase in renal cyst formation.
...
PMID:Renal tubule Na,K-ATPase polarity in glucocorticoid-induced polycystic kidney disease. 838 15

We have observed that in NZBWF1 mice the affinity for L-tryptophan binding to hepatic nuclei in vitro is markedly less than that of Swiss mice. In vitro binding of [3H]tryptophan to hepatic nuclei from both strains was determined without and with unlabeled L-tryptophan (10(-4) mol/L). The relative specific binding of L-tryptophan to hepatic nuclei in vitro was 60.9 +/- 4.4% for Swiss mice and 35.8 +/- 5.4% (P < 0.01) in NZBWF1 mice. The total specific binding (bound radioactivity/mg nuclear protein) of L-tryptophan to hepatic nuclei in vitro was 74.9% (P < 0.05) lower in NZBWF1 mice than in Swiss mice. Other strains (DBA, SJL and BALB/c) had specific binding affinities similar to that of Swiss mice. Serum and hepatic free tryptophan concentrations and hepatic tryptophan dioxygenase activity in mice that were food-deprived overnight or 1 h after tube-feeding L-tryptophan (20 mg/100 g body weight) were similar in the strains of mice. In vitro [14C] leucine incorporation into protein using hepatic microsomes of mice 1 h after tube-feeding L-tryptophan (20 mg/100 g body weight) revealed a significantly greater (P < 0.05) increase relative to food-deprived controls in Swiss mice (76.8 +/- 19.2%) than the increase in NZBWF1 mice (26.5 +/- 2.6%). Nuclear [14C]-labeled RNA release in vitro was increased 77.2 +/- 18.0% by tube-feeding of L-tryptophan in Swiss but only 7.6 +/- 5.8% (P < 0.02) in NZBWF1 mice. Liver nuclear poly(A)-polymerase and nucleoside triphosphatase activities were variably increased by the administration of L-tryptophan in both strains. In summary, compared with Swiss mice, NZBWF1 mice have a lower specific binding affinity for L-tryptophan by hepatic nuclei, and this alteration may account for the other differences in responses to L-tryptophan by the two strains.
...
PMID:Differences in tryptophan binding to hepatic nuclei of NZBWF1 and Swiss mice: insight into mechanism of tryptophan's effects. 903 27


<< Previous 1 2 3 Next >>

---