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

In this study pyruvate kinase, hexokinase and aldolase are investigated in two types of embryonal tumors, neuroblastomas and medulloblastomas; the results are compared with similar studies in gliomas. The activities of hexokinase and pyruvate kinase are significantly decreased in neuroblastomas. In neuroblastoma and medulloblastoma all five forms of pyruvate kinase (K4, K3M, K2M2, KM3 and M4) are present. In contrast, the gliomas investigated are characterized by the presence of mainly K4 and a little K3M. In neuroblastomas, medulloblastomas and gliomas, hexokinase type I is present; in addition, hexokinase type II is present in two medulloblastomas. Aldolase A is the predominant isozyme in all tumors investigated; this is in contrast with normal nervous tissue. It can be concluded that the isozyme characteristics especially of pyruvate kinase from neuroblastomas and medulloblastomas are comparable with similar findings in retinoblastoma; these findings support the hypothesis that these three tumors have a common embryonic origin.
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PMID:Glycolytic enzymes from human neuroectodermal tumors of childhood. 632 86

GLycolytic enzymes were studied from normal human retinas (both fetal and adult) and from retinoblastomas of eight patients and an established retinoblastoma cell line. No significant differences were found between the enzyme activities in the tissues investigated except for hexokinase and pyruvate kinase, which were significantly decreased in the tumor cells. In fetal retina, five different forms of pyruvate kinase could be detected by electrophoresis (K4, K3M, K2M2, KM3, and M4). In adult retina the K4 isozyme is almost absent, while in retinoblastoma the M4 isozyme is hardly present. In the retinoblastoma cell line, the M4 isozyme is completely absent. Alanine inhibition of pyruvate kinase from the retinoblastoma cell line is more inhibited compared to the pyruvate kinase of fetal retina and retinoblastoma and is even more inhibited compared to adult retina. Electrophoresis of aldolase from adult retina revealed the presence of all potential A-C hybrids (A4, A3C, A2C2, AC3, and C4). Fetal retina, however, is characterized by the predominance of the A type. The same patterns were observed in the retinoblastoma cell line and retinoblastoma. However, in other brain tumors, e.g., gliomas of adults, a five-membered A-C hybrid set is found. Electrophoresis of hexokinase from normal fetal and adult retina revealed the predominance of hexokinase type I; retinoblastoma and retinoblastoma cell line are both characterized by the presence of considerable amounts of hexokinase type II. The isozyme shifts in retinoblastoma result in an enzyme pattern identical to that of fetal retina except for the presence of hexokinase type II.
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PMID:Characterization of some glycolytic enzymes from human retina and retinoblastoma. 710 15

In previous studies, we showed that endothelin-1 increased astrocyte proliferation and glucose uptake. These effects were similar to those observed with other gap junction inhibitors, such as carbenoxolone (CBX). Because 24-h treatment with endothelin-1 or CBX downregulates the expression of connexin43, the main protein forming astrocytic gap junctions, which can also be involved in proliferation, in this study, we addressed the possible role of connexin43 in the effects of endothelin-1. To do so, connexin43 was silenced in astrocytes by siRNA. The knock down of connexin43 increased the rate of glucose uptake, characterized by the upregulation of GLUT-1 and type I hexokinase. Neither endothelin-1 nor CBX were able to further increase the rate of glucose uptake in connexin43-silenced astrocytes. In agreement, no effects of endothelin-1 and CBX on GLUT-1 and type I hexokinase were observed in connexin-43 silenced astrocytes or in astrocytes from connexin43 knock-out (KO) mice. Our previous studies suggested a close relationship between glucose uptake and astrocyte proliferation. Consistent with this, connexin43-silenced astrocytes exhibited an increase in Ki-67, a marker of proliferation. The effects of ET-1 on retinoblastoma phosphorylation on Ser780 and on the upregulation of cyclins D1 and D3 were affected by the levels of connexin43. In conclusion, our results indicate that connexin43 participates in the effects of endothelin-1 on glucose uptake and proliferation in astrocytes. Interestingly, although the rate of growth in connexin43 KO astrocytes has been reported to be reduced, we observed that an acute reduction in connexin43 by siRNA increased proliferation and glucose uptake.
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PMID:Connexin43 is involved in the effect of endothelin-1 on astrocyte proliferation and glucose uptake. 1875 37

Microsporidia comprise a large phylum of obligate intracellular eukaryotes that are fungal-related parasites responsible for widespread disease, and here we address questions about microsporidia biology and evolution. We sequenced three microsporidian genomes from two species, Nematocida parisii and Nematocida sp1, which are natural pathogens of Caenorhabditis nematodes and provide model systems for studying microsporidian pathogenesis. We performed deep sequencing of transcripts from a time course of N. parisii infection. Examination of pathogen gene expression revealed compact transcripts and a dramatic takeover of host cells by Nematocida. We also performed phylogenomic analyses of Nematocida and other microsporidian genomes to refine microsporidian phylogeny and identify evolutionary events of gene loss, acquisition, and modification. In particular, we found that all microsporidia lost the tumor-suppressor gene retinoblastoma, which we speculate could accelerate the parasite cell cycle and increase the mutation rate. We also found that microsporidia acquired transporters that could import nucleosides to fuel rapid growth. In addition, microsporidian hexokinases gained secretion signal sequences, and in a functional assay these were sufficient to export proteins out of the cell; thus hexokinase may be targeted into the host cell to reprogram it toward biosynthesis. Similar molecular changes appear during formation of cancer cells and may be evolutionary strategies adopted independently by microsporidia to proliferate rapidly within host cells. Finally, analysis of genome polymorphisms revealed evidence for a sexual cycle that may provide genetic diversity to alleviate problems caused by clonal growth. Together these events may explain the emergence and success of these diverse intracellular parasites.
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PMID:Microsporidian genome analysis reveals evolutionary strategies for obligate intracellular growth. 2281 31