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)

Hereditary non-spherocytary haemolytic anaemias have their cause in enzymopathies of the pentose phosphate cycle and the glycolysis of the erythrocytes. The 11 known enzyme defects of the erythrocytary glycolysis in consequence of the reduced preparation of adenosine triphosphatase condition a deficient stability of the membrane of the erythrocytes. Therefore, the increased autohaemolysis in normal osmotic resistance is a reference to these forms of anaemia, which are particularly to be differentiated from hereditary sperocytoses. In Middle Europe the deficiency of pyruvate kinase plays the greatest part among the otherwise rarely diagnosed enzymopenic haemolytic anaemias.
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PMID:[Defects in erythrocyte glycolysis enzymes as the cause of nonspherocytic hemolytic anemia]. 13 17

Red blood cell plasma membranes contain a number of enzymes: ATPases, anion transport protein, glyceraldehyde 3-phosphate dehydrogenase, protein kinases, adenylate cyclase, acetylcholinesterase. Most of them are tightly bound to the membrane and are present in small amounts. As a result, structural characterization of erythrocyte membrane enzymes has not yet been successful. Functional studies have, however, yielded a great deal of information. ATPases allow active transport of cations (calcium, sodium, potassium). Anion transport protein controls movements of chloride and phosphate ions, and of glucose and water. Among glycolytic enzymes: glyceraldehyde 3-phosphate dehydrogenase is partially bound to the membrane. Protein kinases catalyze the phosphorylation of several membrane proteins, one of which (spectrin) is involved in red blood cell mechanical properties. The physiological role of adenylate cyclase is unknown. Acetylcholinesterase is an ectoenzyme. Calcium-dependent ATPase, adenylate cyclase and phosphorylation of erythrocyte membrane proteins have been found abnormal in various conditions: hereditary spherocytosis, sickle-cell anemia, progressive muscular dystrophies, all of these disorders being associated with a decreased deformability of the erythrocyte.
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PMID:The enzymes of the red blood cell plasma membrane. 14 25

The key to symptomatology in uremia is nitrogen retention leading to amidination and transmidination of a variety of substrates. The product of this activity is a series of guanidino acids which are methyl receptors converting S-adenosylmethionine to adenosine and homocysteine. Adenosine is a potent inhibitor of the enzyme ATPase and, in this way, contributes to the anemia, the bleeding diathesis and the CNS symptoms of uremia. Homocysteine is an inhibitor of pyridoxal phosphate-induced reactions and contributes to the angiitis and thromboembolism so unexpectedly encountered in chronic uremia.
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PMID:Alternate reasons for atherogenesis in uremia. 15 May 96

Previous studies of the expression of SV40 genetic information by skin fibroblasts included limited numbers of cell donors and failed to adequately consider possible effects of age, sex, and ethnic origin on assay results. A population of 76 healthy subjects were selected for study following determination of personal and family disease history and karyological analysis. Skin fibroblasts from these individuals were tested for expression of SV40 T-antigen by indirect immunofluorescent assay. The data were normally distributed and showed no significant differences between the age, sex, or ethnic groups tested. The occurrence of rare karyological anomalies in this control population had no effect on T-antigen expression. Fibroblasts from 10 Fanconi anemia patients demonstrated significantly elevated expression of T antigen compared to the well-defined control population, based on simple statistical criteria. T-antigen expression was elevated in two young patients prior to the onset of anemia and did not appear to correlate with the incidence or severity of other specific symptoms. Thus, elevated T-antigen expression in Fanconi anemia fibroblasts reflects an actual defect at the cellular level, rather than clinical, age, sex or ethnic factors not previously considered.
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PMID:SV40 T-antigen expression in skin fibroblasts from clinically normal individuals and from ten cases of Fanconi anemia. 19 77

Experimental infection of hamsters with Leishmania donovani caused visceral leishmaniasis in which hematological changes occurred. The infected hamsters were anemic and reticulocyte counts were high. No significant change in the serum erythropoietin level was noted. Red cell membrane Na(+)-K(+)-ATPase and acetylcholinesterase activities increased. Osmotic fragility of the erythrocytes from infected animals increased. The level of 2,3-diphosphoglycerate of the red cells increased with the degree of anemia.
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PMID:Anemia in experimental visceral leishmaniasis in hamsters. 131 Jul 31

The influences of iron deficiency on erythrocyte spanning membrane proteins, band 3 protein and Na(+)-K(+)-ATPase, were studied in the growing rats with iron deficient anemia. The main findings were (1) reduction of band 3 and increment of band 4.1 protein. (2) diminished rate constant of pyruvate-chloride exchange (Kp:Cl.h-1) of the erythrocytes and (3) significant decrease of Na(+)-K(+)-ATPase activity only at the early stage of iron exhaustion. In addition, there was a significant negative correlation between Kp:Cl.h-1 and Na(+)-K(+)-ATPase activity both in iron deficient rats and in the controls. It is suggested that the composition and function of the erythrocyte spanning-membrane proteins for ion exchange could be affected by iron deficiency.
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PMID:Abnormalities of ion-exchange proteins of the red cell membrane in iron deficiency anemia. 131 72

The occurrence of auto-antibodies in patients with the autoimmune disease pernicious anaemia and in patients with active duodenal ulcers was investigated. In order to characterize antigenic structures, various cellular and subcellular fractions were prepared from pig gastric mucosa and from a homogenate of duodenal mucosa. By means of an enzyme-linked immunosorbent assay and immunoblotting, both the H+,K(+)-ATPase and pepsinogen/pepsin were shown to constitute the major antigens. All of the seven pernicious-anaemia sera that were tested contained auto-antibodies against both antigens, and the epitopes of the H+,K(+)-ATPase were shown to be localized on its cytoplasmic face. In 75% (18/24) of the sera from patients with duodenal ulcers, auto-antibodies were detected when using purified antigens. Six sera reacted with H+,K(+)-ATPase and twelve reacted with pepsinogen, one reacted with both antigens, and four sera reacted with the duodenal mucosal antigen. The occurrence of auto-antibodies indicates that there is a mucosal lesion and that immunological factors may be involved in the pathogenesis of the disease in some patients.
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PMID:The occurrence of auto-antibodies in patients with gastro-duodenal lesions. 169 83

The influences of iron deficiency on the cochlear iron enzymes and adenosine triphosphatase were studied in 68 iron-deficient rats and 68 control rats (normal and with chronic anemia). A disorderly or topographic distribution and reduction or disappearance of the cochlear succinic dehydrogenase and peroxidase reaction products were found in 37.8% of the rats fed on a basic iron-deficient diet for 14 to 100 days. The activity of cochlear sodium-potassium-dependent adenosine triphosphatase in iron-deficient rats was slightly increased, compared to that in normal controls. These results suggest that iron deficiency would produce significant abnormalities of succinic dehydrogenase and peroxidase activity, which in turn would disturb cell respiration and initiate peroxidative damage to the inner ear cells, result in sensorineural hearing loss, or provide a pathologic basis for cochlear deafness.
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PMID:Changes in the cochlear iron enzymes and adenosine triphosphatase in experimental iron deficiency. 217 94

A mild hereditary nonspherocytic anemia in Beagle dogs was studied. Compared to RBCs from normal dogs, RBCs from hemolytic Beagles were larger on average, contained more potassium, and exhibited an approximately 50% decrease in rate of loss of ATP induced by Ca and the ionophore, A23187. Under certain conditions, this rate of ATP loss can be taken as a measure of the Ca pump ATPase activity of intact RBCs. From RBC fractionation studies it appeared that the defective Ca pump ATPase was acquired during the relatively short life-span of the hemolytic RBC. Significant loss of Ca pump ATPase may be causally related to the hemolytic anemia. The mechanism(s) by which Ca pump ATPase activity is lost in this hemolytic anemia remain(s) to be determined.
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PMID:The activity of the red blood cell Ca pump is decreased in hemolytic anemia of the beagle dog. 252 73

The effect of parathyroid hormone on erythrocytes from newborn and adult rabbits was studied in relation to the fragility pattern in hypotonic salt solutions and the activities of Ca- and Mg-dependent ATPases. Median osmotic fragility of red blood cells from newborn rabbits was significantly higher than in red blood cells from mature rabbits. Parathyroid hormone increased the mean osmotic fragility of red blood cells from newborn and adult rabbits, but showed the greater effect on those from newborns. Similarly, the hormone stimulated to a much greater extent the Ca-ATPase, but not the Mg-ATPase in red blood cells from the newborn rabbits, in comparison with red blood cells from adult rabbits. Parathyroid hormone, which is greatly elevated in the blood of patients with chronic renal failure, may be one cause for the anaemia seen in these patients, and its effect, which is mediated by Ca-ATPase activity, is stronger on young red blood cells. Significant morphological changes in the young red blood cells, observed by scanning electron microscopy, were caused by parathyroid hormone.
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PMID:Effect of parathyroid hormone on the fragility and enzyme activities of red blood cells from young and mature rabbits. 295 52


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