mAcon1

Drosophila melanogaster

Mitochondrial aconitase 1 (mAcon1) encodes an enzyme that harbors an iron-sulfur cluster and catalyses the first step of the Krebs Cycle in mitochondria, converting citrate into isocitrate.

ScsA

Drosophila melanogaster

Succinyl-coenzyme A synthetase beta subunit, ADP-forming (ScsbetaA) encodes a subunit of the ligase that converts succinate to succinyl-CoA in the TCA/Krebs cycle. It contributes to apoptosis and sperm individualization.

Indy

Drosophila melanogaster

I'm not dead yet (Indy) encodes a plasma membrane transporter of Krebs cycle intermediates (citrate, succinate, fumarate, alpha-ketoglutarate) of the SLC13A family that is important in organismal intermediary metabolism. Mutations in Indy create a favorable metabolic state, similar to calorie restriction, and extend life span.

Slc41a1

Mus musculus

PHENOTYPE: Homozygous null mice exhibit partial rescue of the negative effects of magnesium starvation on Krebs cycle enzyme activity in cardiac mitochondria and increased electron transport chain complex I, III, IV, and V activities but decreased complex II activity irrespective of the type of magnesium diet. [provided by MGI curators]

cs

Homo sapiens

The protein encoded by this gene is a Krebs tricarboxylic acid cycle enzyme that catalyzes the synthesis of citrate from oxaloacetate and acetyl coenzyme A. The enzyme is found in nearly all cells capable of oxidative metablism. This protein is nuclear encoded and transported into the mitochondrial matrix, where the mature form is found. [provided by RefSeq, Jul 2008]

Dic1

Drosophila melanogaster

Dicarboxylate carrier 1 (Dic1) encodes a protein of the inner mitochondrial membrane that catalyzes an electroneutral exchange across the inner mitochondrial membrane of dicarboxylates (e.g. malonate, malate, succinate) for inorganic phosphate and certain sulfur-containing compounds (e.g. sulfite, sulfate, thiosulfate). The main role of the product of is in gluconeogenesis. The carrier protein has also an anaplerotic role supplying substrates for the Krebs cycle.

Slc25a10

Homo sapiens

This gene encodes a member of a family of proteins that translocate small metabolites across the mitochondrial membrane. The encoded protein exchanges dicarboxylates, such as malate and succinate, for phosphate, sulfate, and other small molecules, thereby providing substrates for metabolic processes including the Krebs cycle and fatty acid synthesis. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene. [provided by RefSeq, Aug 2012]

Ogdh

Homo sapiens

This gene encodes one subunit of the 2-oxoglutarate dehydrogenase complex. This complex catalyzes the overall conversion of 2-oxoglutarate (alpha-ketoglutarate) to succinyl-CoA and CO(2) during the Krebs cycle. The protein is located in the mitochondrial matrix and uses thiamine pyrophosphate as a cofactor. A congenital deficiency in 2-oxoglutarate dehydrogenase activity is believed to lead to hypotonia, metabolic acidosis, and hyperlactatemia. Alternative splicing results in multiple transcript variants encoding distinct isoforms.[provided by RefSeq, Sep 2009]

Slc13a3

Homo sapiens

Mammalian sodium-dicarboxylate cotransporters transport succinate and other Krebs cycle intermediates. They fall into 2 categories based on their substrate affinity: low affinity and high affinity. Both the low- and high-affinity transporters play an important role in the handling of citrate by the kidneys. The protein encoded by this gene represents the high-affinity form. Alternatively spliced transcript variants encoding different isoforms have been found for this gene, although the full-length nature of some of them have not been characterized yet. [provided by RefSeq, Jul 2008]

fh

Homo sapiens

The protein encoded by this gene is an enzymatic component of the tricarboxylic acid (TCA) cycle, or Krebs cycle, and catalyzes the formation of L-malate from fumarate. It exists in both a cytosolic form and an N-terminal extended form, differing only in the translation start site used. The N-terminal extended form is targeted to the mitochondrion, where the removal of the extension generates the same form as in the cytoplasm. It is similar to some thermostable class II fumarases and functions as a homotetramer. Mutations in this gene can cause fumarase deficiency and lead to progressive encephalopathy. [provided by RefSeq, Jul 2008]