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

BRENDA support

Literature summary for 6.3.1.20 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
Search for more literature for 6.3.1.20

Protein Variants

Protein Variants Comment Organism
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

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

Metals/Ions

Metals/Ions Comment Organism Structure
Mg2+ required Plasmodium berghei

Natural Substrates/ Products (Substrates)

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

Organism

Organism UniProt Comment Textmining
Plasmodium berghei
-
-
-
Plasmodium berghei A0A113RHS8
-
-
Plasmodium berghei ANKA
-
-
-
Plasmodium berghei ANKA A0A113RHS8
-
-

Substrates and Products (Substrate)

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

Synonyms

Synonyms Comment Organism
lipoic acid ligase
-
 Plasmodium berghei
LplA1
-
 Plasmodium berghei
Lpla2
-
 Plasmodium berghei

Cofactor

Cofactor Comment Organism Structure
ATP
-
 Plasmodium berghei

Expression

Organism Comment Expression
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

General Information Comment Organism
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
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
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