Literature summary for 1.3.1.118 extracted from

Gurvitz, A.
Triclosan inhibition of mycobacterial InhA in Saccharomyces cerevisiae Yeast mitochondria as a novel platform for in vivo antimycolate assays (2010), Lett. Appl. Microbiol., 50, 399-405 .

Search for more literature for 1.3.1.118

Cloned(Commentary)

Cloned (Comment)	Organism
expression Saccharomyces cerevisiae etr1D cells lacking Etr1p, the 2-trans-enoyl-thioester reductase of mitochondrial type 2 fatty acid synthase. Yeast mitochondria are used as a surrogate compartment for hosting the drug-target protein InhA from mycobacterial FASII. The heterologous enzyme is ectopically expressed in a yeast mutant strain from which the native gene encoding the corresponding mitochondrial FASII enzyme is missing. Using an appropriate fungal mitochondrial leader sequence, the mycobacterial protein is directed to the mitochondria, where it can rescue the respiratory growth phenotype of the mutant. The rationale behind the assay is that added antimycolates are foreseen to inhibit the mycobacterial enzyme, thereby recreating the respiratory deficiency of the original mutant, discernible as poor colony formation and growth on glycerol medium	Mycobacterium tuberculosis

Cloned (Comment)

Organism

expression Saccharomyces cerevisiae etr1D cells lacking Etr1p, the 2-trans-enoyl-thioester reductase of mitochondrial type 2 fatty acid synthase. Yeast mitochondria are used as a surrogate compartment for hosting the drug-target protein InhA from mycobacterial FASII. The heterologous enzyme is ectopically expressed in a yeast mutant strain from which the native gene encoding the corresponding mitochondrial FASII enzyme is missing. Using an appropriate fungal mitochondrial leader sequence, the mycobacterial protein is directed to the mitochondria, where it can rescue the respiratory growth phenotype of the mutant. The rationale behind the assay is that added antimycolates are foreseen to inhibit the mycobacterial enzyme, thereby recreating the respiratory deficiency of the original mutant, discernible as poor colony formation and growth on glycerol medium

Mycobacterium tuberculosis

Inhibitors

Inhibitors	Comment	Organism	Structure
additional information	the heterologous enzyme is ectopically expressed in a yeast mutant strain from which the native gene encoding the corresponding mitochondrial FASII enzyme is missing.Using an appropriate fungal mitochondrial leader sequence, the mycobacterial protein is directed to the mitochondria, where it can rescue the respiratory growth phenotype of the mutant. The rationale behind the assay is that added antimycolates are foreseen to inhibit the mycobacterial enzyme, thereby recreating the respiratory deficiency of the original mutant, discernible as poor colony formation and growth on glycerol medium	Mycobacterium tuberculosis
triclosan	demonstration of triclosan inhibition of InhA in yeast represents a meaningful variation in studying this effect in mycobacteria, because it occurrs without the potentially confusing aspects of perturbing protein-protein interactions which are presumed vital to mycobacterial FASII, inactivating other important enzymes or eliciting a dedicated transcriptional response in Mycobacterium tuberculosis	Mycobacterium tuberculosis

Organism

Organism	UniProt	Comment	Textmining
Mycobacterium tuberculosis	-	-	-

Synonyms

Synonyms	Comment	Organism
InhA	-	Mycobacterium tuberculosis

General Information

General Information	Comment	Organism
metabolism	the enzyme is involved in mycolic acid biosynthesis. It is part of the dissociative type 2 fatty acid synthase (FASII) system	Mycobacterium tuberculosis