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Literature summary for 2.4.1.345 extracted from

  • Boldrin, F.; Ventura, M.; Degiacomi, G.; Ravishankar, S.; Sala, C.; Svetlikova, Z.; Ambady, A.; Dhar, N.; Kordulakova, J.; Zhang, M.; Serafini, A.; Vishwas, K.G.; Vishwas, V.G.; Kolly, G.S.; Kumar, N.; Palu, G.; Guerin, M.E.; Mikusova, K.; Cole, S.T.; Manganelli, R.
    The phosphatidyl-myo-inositol mannosyltransferase PimA is essential for Mycobacterium tuberculosis growth in vitro and in vivo (2014), J. Bacteriol., 196, 3441-3451.
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
medicine PimA is required for viability during macrophage infection. In two different mouse models of infection a dramatic decrease in viable counts is observed upon silencing of the gene. Depletion of PimA results in complete clearance of the mouse lungs during both the acute and chronic phases of infection Mycobacterium tuberculosis

Cloned(Commentary)

Cloned (Comment) Organism
-
Mycobacterium tuberculosis

Localization

Localization Comment Organism GeneOntology No. Textmining
plasma membrane
-
Mycobacterium tuberculosis 5886
-

Organism

Organism UniProt Comment Textmining
Mycobacterium tuberculosis P9WMZ5
-
-
Mycobacterium tuberculosis H37Rv P9WMZ5
-
-

Synonyms

Synonyms Comment Organism
phosphatidyl-myo-inositol mannosyltransferase
-
Mycobacterium tuberculosis
PimA
-
Mycobacterium tuberculosis
Rv2610c
-
Mycobacterium tuberculosis

General Information

General Information Comment Organism
physiological function downregulation of PimA expression causes bactericidality in batch cultures associated with markedly reduced levels of phosphatidyl-myo-inositol dimannosides. PimA is required for viability during macrophage infection. In two different mouse models of infection a dramatic decrease in viable counts is observed upon silencing of the gene. Depletion of PimA results in complete clearance of the mouse lungs during both the acute and chronic phases of infection Mycobacterium tuberculosis