Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 4.1.3.1 extracted from

  • Eoh, H.; Rhee, K.Y.
    Methylcitrate cycle defines the bactericidal essentiality of isocitrate lyase for survival of Mycobacterium tuberculosis on fatty acids (2014), Proc. Natl. Acad. Sci. USA, 111, 4976-4981.
    View publication on PubMedView publication on EuropePMC

Inhibitors

Inhibitors Comment Organism Structure
Itaconic acid itaconic acid specifically inhibits growth of wild-type cells on acetate and propionate, but not dextrose, in an ICL-dependent manner, and elicited metabolomic changes similar to those observed with ICL-deficient cells. Enzyme ICL inhibition by itaconic acid results in a specific decrease in intrabacterial pH from pH 7.3 to pH 6.4 in propionate-grown cells, not in acetate-grown cells Mycobacterium tuberculosis

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
isocitrate Mycobacterium tuberculosis
-
succinate + glyoxylate
-
?
additional information Mycobacterium tuberculosis Mycobacterium tuberculosis isocitrate lyases are catalytically bifunctional isocitrate and methylisocitrate lyases, EC 4.1.3.1 and EC 4.1.3.30, required for growth on even and odd chain fatty acids ?
-
?

Organism

Organism UniProt Comment Textmining
Mycobacterium tuberculosis
-
-
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
isocitrate
-
Mycobacterium tuberculosis succinate + glyoxylate
-
?
additional information Mycobacterium tuberculosis isocitrate lyases are catalytically bifunctional isocitrate and methylisocitrate lyases, EC 4.1.3.1 and EC 4.1.3.30, required for growth on even and odd chain fatty acids Mycobacterium tuberculosis ?
-
?

Synonyms

Synonyms Comment Organism
ICL
-
Mycobacterium tuberculosis

General Information

General Information Comment Organism
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 Mycobacterium tuberculosis
physiological function Mycobacterium tuberculosis isocitrate lyases are catalytically bifunctional isocitrate and methylisocitrate lyases required for growth on even and odd chain fatty acids Mycobacterium tuberculosis