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Statements

Subject Item
dbr:Cytochalasin_E
rdf:type
yago:WikicatActinInhibitors wikidata:Q11173 dbo:Drug yago:PlantToxin115036638 owl:Thing yago:MolecularFormula106817173 yago:Toxin115034074 dbo:ChemicalCompound yago:Matter100020827 yago:Poison115032376 n18:ChemicalObject dbo:ChemicalSubstance yago:WikicatMycotoxins yago:Inhibitor114724436 yago:Formula106816935 yago:Communication100033020 yago:Abstraction100002137 yago:Message106598915 yago:Substance100020090 yago:WikicatMolecularFormulas yago:Mycotoxin115036536 yago:Statement106722453 yago:PhysicalEntity100001930
rdfs:label
Cytochalasin E
rdfs:comment
Cytochalasin E, a member of the cytochalasin group, is an inhibitor of actin polymerization in blood platelets. It inhibits angiogenesis and tumor growth. Unlike and cytochalasin B, it does not inhibit glucose transport. Cytochalasin E, however, was noted to decrease glucose absorption in mice around the intestinal tissues by increasing the Km needed for glucose to reach the Vmax, which meant that a higher concentration of glucose was required in its presence to attain Vmax. Since Vmax remained the same according to another study, it is evident that CE is indeed a competitive inhibitor at the intestinal receptor sites for glucose.
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dbc:Carbonate_esters dbc:Epoxides dbc:Lactones dbc:Actin_inhibitors dbc:Mycotoxins
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4465739
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1089266802
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Cytochalasin E.png
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-14
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363722351
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dbo:abstract
Cytochalasin E, a member of the cytochalasin group, is an inhibitor of actin polymerization in blood platelets. It inhibits angiogenesis and tumor growth. Unlike and cytochalasin B, it does not inhibit glucose transport. Cytochalasin E, however, was noted to decrease glucose absorption in mice around the intestinal tissues by increasing the Km needed for glucose to reach the Vmax, which meant that a higher concentration of glucose was required in its presence to attain Vmax. Since Vmax remained the same according to another study, it is evident that CE is indeed a competitive inhibitor at the intestinal receptor sites for glucose. Because of its antiangiogenic effect, cytochalasin E is a potential drug for age-related macular degeneration, a kind of blindness caused by an abnormal proliferation of blood vessels in the eye. Cytochalasin E was found to be a potent and selective inhibitor of bovine capillary endothelial (BCE) cell proliferation. Cytochalasin E differs from other cytochalasin molecules by having an epoxide, which is required for specificity and potency. Cytochalasin E is a potent antiangiogenic agent that may be useful for treatments of cancer and other pathologic angiogenesis. Cytochalasin E was also found to inhibit autophagy, a process vital in recycling dysfunctional cells and cellular components. Cancer cells thus favor autophagy due to its role in countering metabolic stresses induced by anti-cancer drugs such as bortezomib in order to regenerate healthier cancer cells for continued proliferation and growth. In a study, it was confirmed that when CE was used, fusion of autophagosomes with lysozyme was inhibited and so cell death due to bortezomib, a proteasome inhibitor, was amplified as unnecessary proteins would continue to build up inside cancer cells unable to be further recycled through autophagy, leading to apoptosis.
gold:hypernym
dbr:Inhibitor
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wikipedia-en:Cytochalasin_E?oldid=1089266802&ns=0
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6351
dbo:iupacName
(4E,6R,8S,10E,11aS,11bS,12aR,13S,13aS,14S)-14-Benzyl-6-hydroxy-6,8,12a,13-tetramethyl-9,11a,11b,12a,13,13a,14,15-octahydro-2H-[1,3]dioxacyclotridecino[4,5-d]oxireno[2,3-f]isoindole-2,7,16(6H,8H)-trione
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wikipedia-en:Cytochalasin_E