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Literature summary extracted from

  • Wang, M.; Wang, Q.; Gao, X.; Su, Z.
    Conditional knock-out of lipoic acid protein ligase 1 reveals redundancy pathway for lipoic acid metabolism in Plasmodium berghei malaria parasite (2017), Parasit. Vectors, 10, 315 .
    View publication on PubMedView publication on EuropePMC

Protein Variants

EC Number Protein Variants Comment Organism
6.3.1.20 additional information generation of conditional knockout lplA1 mutants. An anhydrotetracycline (ATc)-inducible transcription system is used to generate transgenic Plasmodium berghei parasites in which the lplA1 gene is conditionally knocked out (LplA1-cKO), phenotype, overview. LplA1-cKO parasites shows severely impaired growth in vivo in the first 8 days of infection, and retarded blood-stage development in vitro, in the absence of ATc. But these parasites resume viability in the late stage of infection and mounted high levels of parasitemia leading to the death of the hosts Plasmodium berghei

Localization

EC Number Localization Comment Organism GeneOntology No. Textmining
6.3.1.20 mitochondrion
-
 Plasmodium berghei 5739
-

Metals/Ions

EC Number Metals/Ions Comment Organism Structure
6.3.1.20 Mg2+ required Plasmodium berghei

Natural Substrates/ Products (Substrates)

EC Number Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
6.3.1.20 ATP + (R)-lipoate + a [lipoyl-carrier protein]-L-lysine Plasmodium berghei
-
 a [lipoyl-carrier protein]-N6-(lipoyl)lysine + AMP + diphosphate
-
 ?
6.3.1.20 ATP + (R)-lipoate + a [lipoyl-carrier protein]-L-lysine Plasmodium berghei ANKA
-
 a [lipoyl-carrier protein]-N6-(lipoyl)lysine + AMP + diphosphate
-
 ?

Organism

EC Number Organism UniProt Comment Textmining
6.3.1.20 Plasmodium berghei
-
-
-
6.3.1.20 Plasmodium berghei A0A113RHS8
-
-
6.3.1.20 Plasmodium berghei ANKA
-
-
-
6.3.1.20 Plasmodium berghei ANKA A0A113RHS8
-
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
6.3.1.20 ATP + (R)-lipoate + a [lipoyl-carrier protein]-L-lysine
-
 Plasmodium berghei a [lipoyl-carrier protein]-N6-(lipoyl)lysine + AMP + diphosphate
-
 ?
6.3.1.20 ATP + (R)-lipoate + a [lipoyl-carrier protein]-L-lysine
-
 Plasmodium berghei ANKA a [lipoyl-carrier protein]-N6-(lipoyl)lysine + AMP + diphosphate
-
 ?

Synonyms

EC Number Synonyms Comment Organism
6.3.1.20 lipoic acid ligase
-
 Plasmodium berghei
6.3.1.20 LplA1
-
 Plasmodium berghei
6.3.1.20 Lpla2
-
 Plasmodium berghei

Cofactor

EC Number Cofactor Comment Organism Structure
6.3.1.20 ATP
-
 Plasmodium berghei

Expression

EC Number Organism Comment Expression
6.3.1.20 Plasmodium berghei although lplA1 mRNA expression is regulated tightly by anhydrotetracycline (ATc) during the whole course of infection, lplA2 mRNA expression is significantly increased in the late stage of infection only in the LplA1-cKO parasites that are not exposed to anhydrotetracycline up

General Information

EC Number General Information Comment Organism
6.3.1.20 malfunction LplA1-cKO parasites shows severely impaired growth in vivo in the first 8 days of infection, and retarded blood-stage development in vitro, in the absence of ATc. But these parasites resume viability in the late stage of infection and mounted high levels of parasitemia leading to the death of the hosts. The lplA2 gene can be activated as an alternative pathway to compensate for the loss of LplA1 activity and to maintain lipoic acid metabolism Plasmodium berghei
6.3.1.20 physiological function although lplA1 mRNA expression is regulated tightly by anhydrotetracycline (ATc) during the whole course of infection, lplA2 mRNA expression is significantly increased in the late stage of infection only in the LplA1-cKO parasites that are not exposed to anhydrotetracycline Plasmodium berghei
6.3.1.20 physiological function although lplA1 mRNA expression is regulated tightly by anhydrotetracycline (ATc) during the whole course of infection, lplA2 mRNA expression is significantly increased in the late stage of infection only in the LplA1-cKO parasites that are not exposed to anhydrotetracycline. The lplA2 gene can be activated as an alternative pathway to compensate for the loss of LplA1 activity and to maintain lipoic acid metabolism Plasmodium berghei