EC Number   |
General Information |
Reference |
|---|
    4.1.3.1 | evolution |
the enzyme belongs to the isocitrate lyase ICL subfamily 3, one of two eubacterial groups, it has a substitution of M504I compared to the cold-adapted ICLs, rendering is less thermostable, phylogenetic analysis, overview |
-, 727196 |
| 4.1.3.1 | evolution |
the ICL family includes five subfamilies, and the 2-methylisocitrate lyase (MICL) family. The ICL from Pseudomonas aeruginosa (ICL-Pa) is identified in a different ICL node (subfamily 3) than other Pseudomonas ICL enzymes, phylogenetic analysis |
728845 |
| 4.1.3.1 | malfunction |
a mutant deleted of the ICL gene (acuD) is fully virulent in a murine model |
705567 |
| 4.1.3.1 | malfunction |
an aceA mutant displays enhanced biofilm formation during anaerobic growth. Expression of PcrV, of PopN (a regulator of the T3SS translocation process), ExoS (a T3 effector protein), and ExsD (a T3S regulator) is greatly reduced in the aceA mutant. Expression of aceA from a plasmid in trans can restore PcrV expression and ICL activity in the aceA mutant |
728417 |
| 4.1.3.1 | malfunction |
an ICL-deficient mutant is unable to utilize acetate, ethanol, citrate, glycerol, oleate, lactate, pyruvate, peptone, glutamate or alanine for growth, unlike the parental strain. ICL-deficient mutant is unable to utilize nonfermentable carbon sources and has reduced virulence in mice |
705567 |
| 4.1.3.1 | malfunction |
an ICL1 mutant shows the same number of subarachnoidal yeast cells as the wild-type after 10 days in immunosuppressed rabbits. In an inhalation model of murine cryptococcosis, no differences in survival between an ICL1 mutant and the wild-type |
705567 |
| 4.1.3.1 | malfunction |
deletion of the ICL1 gene causes a reduction in appressorium formation, conidiogenesis and cuticle penetration, and an overall decrease in damage to leaves of rice and barley |
705567 |
| 4.1.3.1 | malfunction |
enzyme-deficient cells undergo a progressive depletion of TCA cycle intermediates and accumulation of propionyl-CoA when metabolizing fatty acid substrates, phenotype, overview. Enzyme-deficient cells are unable to metabolize both even- and odd-chain fatty acids because of the dead-end depletion of TCA cycle intermediates by a constitutively active, but broken, methylcitrate cycle. Addition of cobalamin is sufficient to selectively protect ICL-deficient cells from the bactericidal effects of acetate and propionate, and this attenuation is accompanied by a dose-dependent restoration of TCA cycle activity and propionyl-CoA levels |
728701 |
| 4.1.3.1 | malfunction |
enzyme-deficient Mycobacterium tuberculosis strains are significantly more susceptible than wild type to the antibiotics isoniazid, rifampicin, and streptomycin |
-, 748738 |
| 4.1.3.1 | malfunction |
ICL (aceA) mutant displays reduced virulence on alfalfa seedlings and a reduction in histopathology in rat lungs |
705567 |
