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Literature summary for 1.1.3.6 extracted from

  • Liu, J.; Xian, G.; Li, M.; Zhang, Y.; Yang, M.; Yu, Y.; Lv, H.; Xuan, S.; Lin, Y.; Gao, L.
    Cholesterol oxidase from Bordetella species promotes irreversible cell apoptosis in lung adenocarcinoma by cholesterol oxidation (2014), Cell Death Dis., 5, e1372 .
    View publication on PubMedView publication on EuropePMC

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
cholesterol + O2 Bordetella sp.
-
cholest-4-en-3-one + H2O2
-
?

Organism

Organism UniProt Comment Textmining
Bordetella sp.
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
cholesterol + O2
-
Bordetella sp. cholest-4-en-3-one + H2O2
-
?

Synonyms

Synonyms Comment Organism
COD
-
Bordetella sp.
COD-B
-
Bordetella sp.

Cofactor

Cofactor Comment Organism Structure
FAD
-
Bordetella sp.

General Information

General Information Comment Organism
physiological function cholesterol oxidase from Bordetella species promotes irreversible cell apoptosis in lung adenocarcinoma by cholesterol oxidation in vitro and in vivo. COD-B treatment results in JNK and p38 phosphorylation, downregulation of Bcl-2, upregulation of Bax, activated caspase-3 and cytochrome C release, which likely responds to freshly produced hydrogen peroxide that accompanies cholesterol oxidation. COD-B leads to irreversible cell apoptosis by decreasing cholesterol content and increasing reactive oxygen species level. Cholesterol oxidase (COD) is a flavoprotein that catalyzes the oxidation of cholesterol to 4-cholesten-3-one with the reduction of oxygen to hydrogen peroxide. COD can convert membrane cholesterol to 4-cholesten-3-one and can inhibit the formation of lipid rafts. Different from other cholesterol-depleting agents, COD disrupts lipid rafts by displacing cholesterol with 4-cholesten-3-one. COD-B catalyzes the oxidation of membrane cholesterol in lung adenocarcinoma cell. When cells are pretreated with catalase before adding COD-B and cholesterol, the phosphorylation of Akt and ERK1/2 remaines attenuated compared with the group without catalase treatment. Catalase pretreatment also partially blocks the activation of caspase-3, effect of catalase on the COD-B-induced signaling response, overview. COD-B induces the reversible translocation of caveolin-1, which is involved in trafficking membrane cholesterol, in a cholesterol-reversable manner Bordetella sp.