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)

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.
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PMID:Genetic study of cationic ATPase activities and audiogenic seizure susceptibility in recombinant inbred and congenic strains of mice. 614 Dec 22

Much evidence shows that glia regulates the cation and anion content of brain interstitial space. In rats the pH and bicarbonate (HCO3-) concentration of neurons and glia were derived from carbon 14-labeled HCO3- and dimethyloxazolidinedione uptake into brain and cerebrospinal fluid. Acetazolamide increases the total CO2 concentration in neurons and decreases the pH and HCO3- concentration in glia. Inhibition of glial carbonic anhydrase (CA) reduces conversion of neuronally derived CO2 to HCO3-, glial pH is lowered, and neuronal CO2 accumulates. CA therefore has an essential role in regulating pH in neurons, glia, and interstitial fluid. In audiogenic seizure mice, glial CA activity is increased and glial anion transport is reduced. As the mice age, seizure susceptibility, the increased CA activity, and the defect in anion transport disappear concurrently. The enhanced CA activity in the glial cells of these mice is an adaptive mechanism to overcome the defect in anion transport that results from a deficiency of HCO3- -dependent and Na+- and K+ -dependent adenosine triphosphatase. Pentylenetetrazol stimulates neurons in neonatal rats, but after 10 days of age, when glia is present, it too is stimulated and the seizures are attenuated. Cobalt implantation in the cortex of rats also induces a glial response that ameliorates the focal seizures produced by this procedure.
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PMID:Ionic and acid-base regulation of neurons and glia during seizures. 615 Jun 82

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.
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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

The human lymphoid cell activation antigen CD39 is a known E-type apyrase that hydrolyzes extracellular ATP and ADP, a function important in homotypic adhesion, platelet aggregation, and removal by activated lymphocytes of the lytic effect of ATP. The recently identified putative rat homologue of CD39L1 has been shown to have E-type ecto-ATPase activity, by hydrolyzing extracellular ATP. We have characterized three novel CD39-like transcripts, CD39L2, CD39L3, and CD39L4, which share extensive amino acid homology with other nucleotide triphosphatases in vertebrates, invertebrates, and plants, suggesting that these genes also encode proteins with ecto-nucleotidase activity. Isolation and sequencing of full-length cDNA clones for each gene identified putative proteins of 485, 529, and 429 amino acids. The expression pattern of all five human members of the gene family was analyzed. CD39L2, CD39L3, and CD39L4 were mapped on the human genome, and the murine homologues identified with the putative map locations were assigned on the basis of regions of conserved gene order between human and mouse chromosomes. The map location of mcd39l4 places the gene within a region associated with audiogenic seizure susceptibility in mouse. This disorder is characterized by convulsions induced by loud high-frequency sound and has been shown to be associated with increased nucleotide triphosphatase activity.
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PMID:The CD39-like gene family: identification of three new human members (CD39L2, CD39L3, and CD39L4), their murine homologues, and a member of the gene family from Drosophila melanogaster. 967 30

Here, the genetic context for the study of audiogenic seizures is four single-gene, spontaneous mutations that occurred in the Behavior Genetics Laboratory at the University of Chicago from 1959 to 1969. Three of these increased the incidence of audiogenic seizures, and one of these decreased the incidence of audiogenic seizures. The genetics of one of these mutants is described in detail, and the effect of diet on the same mutant is also described in detail. Research on genetic and environmental effects on the cortical EEG of audiogenic seizures is reviewed; this research included two of these mutants. The cortical EEG associated with audiogenic seizures in this study was consistent with audiogenic seizures being a type of brain stem epilepsy as had been proposed by others. Also, I proposed that brain stem pathophysiology is the same regardless of the genetic or environmental pathway to audiogenic seizure susceptibility. Research is also reviewed using these mutants to determine whether or not a strain association between glutamic acid decarboxylase (GAD) activity in whole brain and susceptibility to audiogenic seizures is pleiotropic and whether or not a strain association between nucleoside triphosphatase (NTPase) activity in the granule cell layer of the dentate fascia of the hippocampus and susceptibility to audiogenic seizures is a lineal or collateral pleiotropy. Lastly, pleiotropy as an explanation for strain comorbidities in aggressive behavior and audiogenic seizures is considered. This article is part of a Special Issue entitled "Genetic and Reflex Epilepsies, Audiogenic Seizures and Strains: From Experimental Models to the Clinic".
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PMID:A genetic context for the study of audiogenic seizures. 2690 25