6.2.1.4: succinate-CoA ligase (GDP-forming)
This is an abbreviated version!
For detailed information about succinate-CoA ligase (GDP-forming), go to the full flat file.
Word Map on EC 6.2.1.4
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6.2.1.4
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tricarboxylic
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tca
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malate
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sucla2
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citric
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mtdna
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methylmalonic
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krebs
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alpha-ketoglutarate
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adp-forming
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substrate-level
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fumarase
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aciduria
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hydrogenosomes
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dguok
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phosphohistidine
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coa-transferase
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phosphoenzyme
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encephalomyopathic
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nishimura
- 6.2.1.4
-
tricarboxylic
- tca
- malate
- sucla2
-
citric
- mtdna
-
methylmalonic
-
krebs
- alpha-ketoglutarate
-
adp-forming
-
substrate-level
- fumarase
-
aciduria
- hydrogenosomes
- dguok
-
phosphohistidine
-
coa-transferase
- phosphoenzyme
-
encephalomyopathic
-
nishimura
Reaction
Synonyms
ATP-specific SCS, G-SCS, G-STK, G-SUCL, GDP-forming SUCL, GTP-dependent succinate:CoA ligase, GTP-forming SUCL, GTP-specific succinate:CoA ligase, GTP-specific succinyl-CoA synthetase, GTP-specific SUCL, GTPSCS, SCS, SCS-alpha, SCS-beta, SCS-betaG, ScsA, SCSalpha, SucCDAm, Succinate thiokinase, succinate-CoA ligase, Succinic thiokinase, Succinyl CoA synthetase, Succinyl coenzyme A synthetase, Succinyl coenzyme A synthetase (GDP-forming), Succinyl coenzyme A synthetase (guanosine diphosphate-forming), succinyl-CoA synthase, Succinyl-CoA synthetase, Succinyl-CoA synthetase (GDP-forming), succinyl-CoA synthetase subunit beta, succinyl-coenzyme A synthetase, SUCL, SUCLG1, SUCLG2, Synthetase, succinyl coenzyme A (guanosine diphosphate-forming)
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6.2.1.4 succinate-CoA ligase (GDP-forming)Advanced search results
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Engineering on EC 6.2.1.4 - succinate-CoA ligase (GDP-forming)
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
K46E/K114D
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the double mutant shows reduced activity with ATP and high specificity towards GTP compared to the wild type enzyme
K46E/K114D/V113L/L227F
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the quadruple mutant shows no activity with ATP and high activity towards GTP compared to the wild type enzyme
V113L/L227F
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the double mutant shows increased activity with ATP compared to the wild type enzyme
K46E/K114D
Blastocystis hominis NandII
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the double mutant shows reduced activity with ATP and high specificity towards GTP compared to the wild type enzyme
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K46E/K114D/V113L/L227F
Blastocystis hominis NandII
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the quadruple mutant shows no activity with ATP and high activity towards GTP compared to the wild type enzyme
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V113L/L227F
Blastocystis hominis NandII
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the double mutant shows increased activity with ATP compared to the wild type enzyme
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A209E
the mutation is associated with encephalomyopathic mitochondrial DNA depletion syndrome
E263K
the mutation is associated with encephalomyopathic mitochondrial DNA depletion syndrome
H71R
the mutation is associated with encephalomyopathic mitochondrial DNA depletion syndrome
V330M
the mutant exhibits an about 10fold higher Km value for succinate compared to the wild type enzyme
additional information
additional information
transposon mutagenesis and deletion of gene sucCD, accumulation of 3SP during 3,3'-dithiodipropionic acid degradation occurs in Tn5::mob-induced mutants of Advenella mimigardefordensis strain DPN7T disrupted in sucCD and in the defined deletion mutant Advenella mimigardefordensis DELTAsucCD
additional information
transposon mutagenesis and deletion of gene sucCD, accumulation of 3SP during 3,3'-dithiodipropionic acid degradation occurs in Tn5::mob-induced mutants of Advenella mimigardefordensis strain DPN7T disrupted in sucCD and in the defined deletion mutant Advenella mimigardefordensis DELTAsucCD
additional information
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transposon mutagenesis and deletion of gene sucCD, accumulation of 3SP during 3,3'-dithiodipropionic acid degradation occurs in Tn5::mob-induced mutants of Advenella mimigardefordensis strain DPN7T disrupted in sucCD and in the defined deletion mutant Advenella mimigardefordensis DELTAsucCD
additional information
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transposon mutagenesis and deletion of gene sucCD, accumulation of 3SP during 3,3'-dithiodipropionic acid degradation occurs in Tn5::mob-induced mutants of Advenella mimigardefordensis strain DPN7T disrupted in sucCD and in the defined deletion mutant Advenella mimigardefordensis DELTAsucCD
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additional information
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the severe disorder in patients with SUCLG1 mutations is likely caused by the absence of both ASUCL and G-SUCL, and thereby a compromised formation of both ATP and GTP. Severe lactic acidosis is found in patients with SUCLG1 mutations, phenotype, overview
additional information
the severe disorder in patients with SUCLG1 mutations is likely caused by the absence of both ASUCL and G-SUCL, and thereby a compromised formation of both ATP and GTP. Severe lactic acidosis is found in patients with SUCLG1 mutations, phenotype, overview
additional information
the severe disorder in patients with SUCLG1 mutations is likely caused by the absence of both ASUCL and G-SUCL, and thereby a compromised formation of both ATP and GTP. Severe lactic acidosis is found in patients with SUCLG1 mutations, phenotype, overview
additional information
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the GDP-dependent isozyme SUCLG2, EC 6.2.1.5, can complement the SUCLA2-related mitochondrial DNA depletion syndrome, a result of mutations in the beta subunit of the ADP-dependent isoform SUCLA2, EC 6.2.1.4
additional information
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naturally occuring mutation c.113_114delAT causes succinate-CoA ligase deficiency
additional information
naturally occuring mutation c.113_114delAT causes succinate-CoA ligase deficiency
additional information
naturally occuring mutation c.113_114delAT causes succinate-CoA ligase deficiency
additional information
construction of a conditional knock-out mutant for the succinyl-CoA synthetase ScsA, depletion mutant displays a 30% reduction in growth rate, which can be restored by supplementation with 0.002 mM succinate in the tissue culture medium, the mitochondrial membrane potential in these parasites is unaltered, lack of a more severe phenotype, overview
additional information
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construction of a conditional knock-out mutant for the succinyl-CoA synthetase ScsA, depletion mutant displays a 30% reduction in growth rate, which can be restored by supplementation with 0.002 mM succinate in the tissue culture medium, the mitochondrial membrane potential in these parasites is unaltered, lack of a more severe phenotype, overview
