Localization | Comment | Organism | GeneOntology No. | Textmining |
---|---|---|---|---|
extracellular | - |
Mycobacterium tuberculosis | - |
- |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
cholesterol + O2 | Mycobacterium tuberculosis | - |
cholest-4-en-3-one + H2O2 | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Mycobacterium tuberculosis | - |
- |
- |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
cholesterol + O2 | - |
Mycobacterium tuberculosis | cholest-4-en-3-one + H2O2 | - |
? |
Synonyms | Comment | Organism |
---|---|---|
CHOD | - |
Mycobacterium tuberculosis |
Cofactor | Comment | Organism | Structure |
---|---|---|---|
FAD | - |
Mycobacterium tuberculosis |
General Information | Comment | Organism |
---|---|---|
malfunction | intracellular replication of an Mycobacterium tuberculosis mutant lacking a functional choD gene (DELTAchoD) is less efficient in macrophages than that of the wild-type strain. In contrast to wild-type tb, the DELTA strain inducesnitric oxide production in macrophages, an action that depends on the TLR2, but not the CR3, signaling pathway. Both wild-type and mutant strains inhibit the production of reactive oxygen species, but the DELTAchoD strain does so to a significantly lesser extent. Blocking TLR2-mediated signaling abolishes the inhibitory effect of wild-type Mycobacterium tuberculosis on reactive oxygen species production by macrophages. The mutant DELTAchoD strain, does not decrease phorbol myristate acetate-induced phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) ib contrast to the wild-type. The production of interleukin 10 by macrophages is significantly lower in DELTAchoD-infected macrophages than in wild-type Mtb-infected macrophages | Mycobacterium tuberculosis |
physiological function | cholesterol oxidase ChoD is capable of modifying the bactericidal and pro-inflammatory activity of human macrophages. and is indispensable in the pathogenesis of Mycobacterium tuberculosis. The enzyme is enzyme capable of converting cholesterol to its 3-keto-4-ene derivative, cholestenone. The wild-type strain inhibits the production of reactive oxygen species. Wild-type Mycobacterium tuberculosis, but not the DELTAchoD strain, decreases phorbol myristate acetate-induced phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2), which are involved in both TLR2-and CR3-mediated signaling pathways | Mycobacterium tuberculosis |