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Literature summary extracted from

  • Bellerose, M.M.; Baek, S.H.; Huang, C.C.; Moss, C.E.; Koh, E.I.; Proulx, M.K.; Smith, C.M.; Baker, R.E.; Lee, J.S.; Eum, S.; Shin, S.J.; Cho, S.N.; Murray, M.; Sassetti, C.M.
    Common variants in the glycerol kinase gene reduce tuberculosis drug efficacy (2019), mBio, 10, e00663-19 .
    View publication on PubMedView publication on EuropePMC

Application

EC Number Application Comment Organism
2.7.1.30 diagnostics frameshift mutations in a hypervariable homopolymeric region of the glpK gene are a specific marker of multidrug resistance in clinical Mycobacterium tuberculosis isolates, and these loss-of-function alleles are also enriched in extensively drug-resistant clones. Drug examples are isoniazid (INH), rifampin (RIF), pyrazinamide (PZA), and ethambutol (EMB) Mycobacterium tuberculosis

Cloned(Commentary)

EC Number Cloned (Comment) Organism
2.7.1.30 gene glpK, genotyping Mycobacterium tuberculosis

Protein Variants

EC Number Protein Variants Comment Organism
2.7.1.30 additional information frameshift mutations in a hypervariable homopolymeric region of the glpK gene are a specific marker of multidrug resistance in clinical Mycobacterium tuberculosis isolates, and these loss-of-function alleles are also enriched in extensively drug-resistant clones. Reversible high-frequency variation in carbon metabolic pathways can produce phenotypically drug-tolerant clones and have a role in the development of resistance. Construction of a DELTAglpK mutant, that is significantly less sensitive to isoniazid (INH) and rifampin (RIF) than the wild-type or the complemented mutant Mycobacterium tuberculosis

Organism

EC Number Organism UniProt Comment Textmining
2.7.1.30 Mycobacterium tuberculosis P9WPK1
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2.7.1.30 Mycobacterium tuberculosis H37Rv P9WPK1
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Synonyms

EC Number Synonyms Comment Organism
2.7.1.30 GLPK
-
 Mycobacterium tuberculosis

General Information

EC Number General Information Comment Organism
2.7.1.30 malfunction frequently observed variation in the glpK coding sequence produces a drug-tolerant phenotype that can reduce antibiotic efficacy and may contribute to the evolution of resistance. Common variation in a homopolymeric region in the glpK gene is associated with drug resistance in clinical isolates. Glycerol catabolic defects are associated with extensive drug resistance in Korea. A panel of Korean Mycobacterium tuberculosis isolates that vary in drug sensitivity profiles, from fully sensitive strains to extensively evolved clones that are phenotypically resistant to more than ten different antibiotics. GlpK frameshift mutations are common in Mycobacterium tuberculosis isolates and associated with drug resistance in Peru Mycobacterium tuberculosis
2.7.1.30 metabolism Mycobacterium tuberculosis genes that alter the rate of bacterial clearance in drug-treated mice. Several functionally distinct bacterial genes are found to alter bacterial clearance, and prominent among these is the glpK gene that encodes the glycerol-3-kinase enzyme that is necessary for glycerol catabolism. Growth on glycerol generally increases the sensitivity of Mycobacterium tuberculosis to antibiotics in vitro, and glpK-deficient bacteria persist during antibiotic treatment in vivo, particularly during exposure to pyrazinamide-containing regimens. Reversible high-frequency variation in carbon metabolic pathways can produce phenotypically drug-tolerant clones and have a role in the development of resistance. The glycerol metabolism increases drug efficacy in vitro and during murine infection, overview Mycobacterium tuberculosis