Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.1.1 (hexokinase)
 5,274 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Streptozotocin treatment (125 mg/kg) in the Chinese hamster induced hyperglycaemia, hypoinsulinaemia, hyperglucagonaemia and changes in body, liver, pancreas, stomach, kidney and adipose tissue weights. The pancreatic reserves of insulin and glucagon in the diabetic animals were low, but stomach glucagon high. These animals showed high levels of phosphoenolpyruvate carboxykinase and low levels of glucokinase, hexokinase, isocitrate dehydrogenase and malic enzyme, but normal levels of pyruvate kinase in the liver. Increases in lactate dehydrogenase subunit B and isozymes 2, 3 and 4 were also observed in the liver, but not in the epididymal fat pad, of the diabetic animals. N-Acetyl-beta-D-glucosaminidase was elevated in plasma, liver and heart, but not in the kidney of the treated animals. Renal alpha-galactosidase and beta-glucosidase were depressed, whereas beta-galactosidase and alpha-glucosidase remained essentially normal. These features indicated that there were considerable differences between the biochemical disorders associated with streptozotocin-diabetes in the Chinese hamster and the published observations in the rat.
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PMID:Streptozotocin-induced diabetes in the Chinese hamster. Biochemical and endocrine disorders. 59 Jun 51

Previously, we described a mutation glr1-1 in Saccharomyces carlsbergensis which pleiotropically relieves the synthesis of the following enzymes from glucose repression: maltase, galactokinase, alpha-galactosidase, NADH:cytochrome c reductase, and cytochrome c oxidase (C. A. Michels and A. Romanowski, J. Bacteriol, 143:674-679, 1980.) In this report, we demonstrate that glr1-1 and two other alleles, glr1-3 and glr1-16, are also insensitive to the glucose repression of invertase synthesis. Determinations of the levels of hexokinase activity and the rate of glucose transport in these mutants show that both are reduced as compared with the parent strain. Complementation tests and genetic analysis indicate that the glr1 mutations are allelic to HXK2, the structural gene for hexokinase B. The significance of this result is discussed with regard to the mechanism of glucose repression in S. carlsbergensis.
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PMID:Pleiotropic mutations regulating resistance to glucose repression in Saccharomyces carlsbergensis are allelic to the structural gene for hexokinase B. 684 88

alpha-Galactosidase activity (alpha- d-galactoside galactohydrolase, EC 3.2.1.22) increased during dark-induced senescence in primary foliage leaves of barley ( Hordeum vulgare L. cv. Steffi). The changes in activity were accompanied by parallel changes in expression of the HvSF11 gene encoding a putative alpha-galactosidase. The transcript level of HvSF23 encoding a second putative alpha-galactosidase stayed constant during leaf senescence. Both alpha-galactosidase activity and the level of the HvSF11 transcript decreased after exogenous application of sucrose and glucose to detached dark-incubated leaves. In contrast, the HvSF23 transcript level was not influenced by sugars. Application of glucose analogs to detached and dark-incubated leaves revealed that phosphorylation of hexose by hexokinase modulates both the alpha-galactosidase activity and the expression of HvSF11. These results indicate that the expression of the genes coding for two alpha-galactosidase isoenzymes is regulated by different signalling pathways, suggesting different functions for the two gene products.
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PMID:Regulation of alpha-galactosidase gene expression in primary foliage leaves of barley ( Hordeum vulgare L) during dark-induced senescence. 1465 58