Malate-aspartate shuttle (WP4315)

Homo sapiens

The malate-aspartate shuttle (sometimes also the malate shuttle) is a biochemical system for translocating electrons produced during glycolysis across the semipermeable inner membrane of the mitochondrion for oxidative phosphorylation in eukaryotes. These electrons enter the electron transport chain of the mitochondria via reduction equivalents to generate ATP. The shuttle system is required because the mitochondrial inner membrane is impermeable to NADH, the primary reducing equivalent of the electron transport chain. To circumvent this, malate carries the reducing equivalents across the membrane. https://en.wikipedia.org/wiki/Malate-aspartate_shuttle

Authors

Amadeo , Kristina Hanspers , Susan Coort , and Eric Weitz

Activity

last edited

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Organisms

Homo sapiens

Communities

Annotations

Pathway Ontology

citric acid cycle pathway classic metabolic pathway citric acid cycle pathway

Participants

Label Type Compact URI Comment
Aspartate Metabolite hmdb:HMDB0006483
Glutamate Metabolite hmdb:HMDB0000148
a-Ketoglutarate Metabolite hmdb:HMDB0000208
Oxalacetate Metabolite hmdb:HMDB0000223
(S)-malate Metabolite hmdb:HMDB0000156
Aspartate Metabolite hmdb:HMDB0006483
Glutamate Metabolite hmdb:HMDB0000148
a-Ketoglutarate Metabolite hmdb:HMDB0000208
Oxalacetate Metabolite hmdb:HMDB0000223
(S)-malate Metabolite hmdb:HMDB0000156
SLC25A11 GeneProduct ensembl:ENSG00000108528
GLAST GeneProduct ensembl:ENSG00000079215
GOT2 GeneProduct ensembl:ENSG00000125166
MDH1 GeneProduct ensembl:ENSG00000014641
GOT2 GeneProduct ensembl:ENSG00000125166
MDH1 GeneProduct ensembl:ENSG00000014641

References

  1. Role of the malate-aspartate shuttle on the metabolic response to myocardial ischemia. Lu M, Zhou L, Stanley WC, Cabrera ME, Saidel GM, Yu X. J Theor Biol. 2008 Sep 21;254(2):466–75. PubMed Europe PMC Scholia
  2. Arginine Methylation of MDH1 by CARM1 Inhibits Glutamine Metabolism and Suppresses Pancreatic Cancer. Wang YP, Zhou W, Wang J, Huang X, Zuo Y, Wang TS, et al. Mol Cell. 2016 Nov 17;64(4):673–87. PubMed Europe PMC Scholia