Plays a key role in glycolysis and gluconeogenesis. In addition, may also function as scaffolding protein.
Carbohydrate degradation; glycolysis; D-glyceraldehyde 3-phosphate and glycerone phosphate from D-glucose: step 4/4.
Involvement in disease
Defects in ALDOA are the cause of glycogen storage disease type 12 (GSD12) [MIM:611881]; also known as red cell aldolase deficiency. A metabolic disorder associated with increased hepatic glycogen and hemolytic anemia. It may lead to myopathy with exercise intolerance and rhabdomyolysis.
Belongs to the class I fructose-bisphosphate aldolase family.
Flow cytometry analysis of MCF-7 (Human breast adenocarcinoma epithelial cell) cells labeling Aldolase (red) with ab169544 at a 1/230 dilution. Cells were fixed with 80% methanol and permeabilized with 0.1% Tween-20. A goat anti-rabbit IgG (Alexa Fluor® 488) (ab150077) was used as the secondary antibody at a 1/2000 dilution. Black - Rabbit monoclonal IgG (Black) (ab172730). Blue (unlabeled control) - Cell without incubation with primary antibody and secondary antibody (Blue).
Zeng Y et al. G6PC3, ALDOA and CS induction accompanies mir-122 down-regulation in the mechanical asphyxia and can serve as hypoxia biomarkers. Oncotarget7:74526-74536 (2016).
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Godar RJ et al. Repetitive stimulation of autophagy-lysosome machinery by intermittent fasting preconditions the myocardium to ischemia-reperfusion injury. Autophagy11:1537-60 (2015).
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