Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hepatocyte and haematopoietic cell contents of the liver of the foetal guinea pig were measured over the latter half of gestation. Hepatocytes represented about 30% of liver volume at mid-gestation and this increased to 70-80% by term; cell volume remained fairly constant until 5-7 days before term, then more than doubled. Haematopoietic cells represented about 5% of liver volume at mid-gestation and this progressively fell to <1% by term. At 75% of gestation hepatocytes and haematopoietic cells were prepared from perfused foetal livers by collagenase digestion. Enzyme activity of the hepatocyte was, without exception, similar to that of the whole liver. In general, enzyme activity in the haematopoietic cells was similar to that in erythrocytes, with relatively low values for aldolase, glycerol 3-phosphate dehydrogenase, phosphoglycerate mutase, enolase, lactate dehydrogenase, phosphoenolpyruvate carboxykinase, fructose 1,6-bisphosphatase, isocitrate dehydrogenase, ;malic' enzyme, glutamate dehydrogenase and aspartate aminotransferase. The haematopoietic cell contribution to total enzyme activity in the foetal liver was usually much less than 10% and could thus not account for the major changes in hepatic enzyme activity over the latter half of gestation. Hepatocytes contained hexokinase isoenzymes I and III, aldolase isoenzymes A and B and pyruvate kinase isoenzymes 1, 2 and 4. The haematopoietic cells contained hexokinase isoenzyme I and two additional bands of activity with slightly greater mobility, aldolase isoenzyme A and pyruvate kinase isoenzymes 2 and 4.
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PMID:The distribution of enzyme and isoenzyme activities between parenchymal and haematopoietic cells in the liver of the foetal guinea pig. 43 88

1. The effects of protein concentration and ionic strength on the adsorption of the individual glycolytic enzymes to F-actin and F-actin--trypomyosin--troponin have been studied. 2. Appreciable association was demonstrated under conditions of physiological ionic strength and high protein concentration, and tropomyosin--troponin established as an important and generalized component of these interactions. 3. Phosphofructokinase, aldolase, pyruvate kinase, lactate dehydrogenase, glyceraldehyde-3-phosphate dehydrogenase and glucose-6-phosphate isomerase were strongly bound under these conditions, while triosephosphate isomerase, phosphoglycerate kinase, phosphoglycerate mutase, enolase and hexokinase displayed less adsorption to the structural proteins. 4. The influence of a number of parameters on the adsorption phenomena was examined. Ca2+ and fructose 1,6-diphosphate increased the adsorption of aldolase, lactate dehydrogenase and pyruvate kinase, while decreasing the adsorption of the enzymes of the constant-proportion group. 5. Of the other major enzymic components of skeletal muscle, creatine kinase, adenylate kinase and malate dehydrogenase showed no adsorption to F-actin--tropomyosin--troponin under the experimental conditions. Some adsorption was evident, however, in the case of aspartate aminotransferase, (NADP) isocitrate dehydrogenase and alpha-glycerolphosphate dehydrogenase. 6. These results have been discussed in relation to their functional significance and the roles of enzyme compartmentation in the cell.
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PMID:On the association of glycolytic enzymes with structural proteins of skeletal muscle. 111 88

Trisomy 19 (Ts19), the only murine trisomy compatible with survival beyond birth, allows systematic studies on the effect of an additional chromosome upon postnatal development. In this review, developmental consequences of murine Ts19 are presented. In Ts19 mice, viability is limited to a few weeks postpartum. Body weight is markedly reduced. The occurrence of malformations of the cardiovascular, skeletal and central nervous systems depends on the parental genetic background. In all organ systems examined, development is delayed by 1-2 days. Ts19 hematopoietic cells exhibit the same survival rate in lethally irradiated hosts as controls. In the CNS, morphological and morphometric studies fail to detect cytoarchitectonic abnormalities: the orderly pattern of development is not disturbed in the visual cortex, cerebellum, locus coeruleus (LC), optic nerve and retina; but neurogenesis, gliogenesis, myelination and invasion of blood vessels are each delayed by 1-2 days. In addition, size and cell number of different brain regions are reduced to a variable degree: the telencephalon and the cerebellar vermis are markedly hypoplastic, whereas the LC, the optic nerve and the retina are hardly reduced in size. Choline acetyltransferase activity is selectively reduced in the Ts19 telencephalon, whereas the activity of the marker enzyme of the GABAergic system is decreased in all brain regions examined. In behavioral tests, visual capacities and orientation ability of Ts19 mice develop with a 2-day delay, while motor coordination is more severely retarded; there is no response to auditory stimulation. Fetal Ts19 ovaries show excessive oocyte degeneration. Development of the testes is only disturbed postnatally: differentiation of gonocytes to A spermatogonia and formation of B spermatogonia are severely disrupted, resulting in a striking reduction in germ cell number and a predominance of Sertoli cells. Histopathological changes exhibit marked intra- and interindividual variations. In addition, growth and lumen formation are impaired in the seminiferous tubules. The proliferative capacity of cultured Ts19 cells is not altered. The activities of glutamate oxaloacetate transaminase-1 and phosphoglycerate mutase-1 are increased by 50%, compatible with a gene dosage effect of these two enzymes. Ganglioside composition is altered in the Ts19 liver, but not in the brain, spleen and heart. Two-dimensional protein patterns show both chromosome-specific and chromosome-nonspecific changes, their frequency being far lower than expected from the number of proteins coded on chromosome 19. Possible pathogenetic mechanisms are discussed.
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PMID:Developmental characteristics of trisomy 19 mice. 781 12