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:2.7.1.1 (
hexokinase
)
5,274
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
A quantitative enzyme analysis of 32 fetal human brains of 6--42 weeks gestational age range was carried out for the major glycolytic and pentose phosphate shunt enzymes. A critical period of raised enzyme levels was observed at 14 weeks. The glycolytic rate was probably controlled by the activities of
hexokinase
and phosphofructokinase which appear from the development patterns to have independent genetic sites. A rise in most enzyme activities was experienced in the final weeks of gestation towards levels consistent with those of adult tissues.
Pentose
phosphate shunt enzyme levels remained virtually unchanged during gestation after 14 weeks.
...
PMID:The development of glycolytic and pentose phosphate shunt enzymes in human brain. 14 Jul 9
Selected aspects of the metabolism of Plasmodium falciparum are reviewed, but conclusions based on the study of other species of plasmodia are intentionally not included since these may not be applicable. The parasites increase glucose consumption 50-100 fold as compared to uninfected red cells; most of the glucose is metabolized to lactic acid. The parasite contains a complete set of glycolytic enzymes. Some enzymes such a
hexokinase
, enolase and pyruvate kinase are vastly increased over corresponding levels in uninfected red cells. However, the pathway for synthesizing 2,3-diphosphoglycerate (2,3-DPG) is absent. Parasitized red cells show a decline in the concentration of 2,3-DPG which may function as an inhibitor for certain essential enzyme pathways.
Pentose
shunt activity is increased in absolute terms, but as a percent of total glucose consumption, there is a decrease during parasite infection of the red cell. The parasite contains a gene for G6PD and can produce a small quantity of parasite-encoded enzyme. It is not clear if the production of this enzyme can be up-regulated in G6PG deficient host red cells. The NADPH normally produced by the pentose shunt can be obtained from other parasite pathways (such as glutamate dehydrogenase). NADPH may subserve additional needs in the infected red cell such as driving diribonucleotide reductase activity--a rate limiting enzyme in DNA synthesis. The role of NADPH in protecting the parasite-red cell system against oxidative stress (via glutathione reduction) remains controversial. Parasitized red cells contain about 10 times more NAD(H) than uninfected red cells, but the NADP(H) content is unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Plasmodium falciparum carbohydrate metabolism: a connection between host cell and parasite. 225 22