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Literature summary for 1.1.1.21 extracted from

  • D'Souza, D.R.; Salib, M.M.; Bennett, J.; Mochin-Peters, M.; Asrani, K.; Goldblum, S.E.; Renoud, K.J.; Shapiro, P.; Passaniti, A.
    Hyperglycemia regulates RUNX2 activation and cellular wound healing through the aldose reductase polyol pathway (2009), J. Biol. Chem., 284, 17947-17955.
    View publication on PubMedView publication on EuropePMC
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Protein Variants

Protein Variants Comment Organism
additional information enzyme downregulation by specific AR-targeted siRNA transfection Homo sapiens

Inhibitors

Inhibitors Comment Organism Structure
Alrestatin inhibits aldose reductase, does not appear to affect RUNX2 activation in cells exposed to euglycemia Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
bone marrow bone marrow endothelial, HBME, cells Homo sapiens
-
endothelial cell
-
 Homo sapiens
-

Synonyms

Synonyms Comment Organism
aldose reductase
-
 Homo sapiens

General Information

General Information Comment Organism
additional information inverse relationship between RUNX2 activity and AR expression, which is induced by hyperglycemia and supports a role for AR in the suppression of RUNX2 activity under hyperglycemic conditions Homo sapiens
physiological function the aldose reductase polyol pathway contributes to microvascular complications since the enzyme mediates vascular damage in response to hyperglycemia. Inhibition of AR reverses hyperglycemic suppression of RUNX2, and it also negatively regulates RUNX2-dependent vascular remodeling in an endothelial cell wounded monolayer assay, which is reversed by specific AR inhibition in hyperglycemia. RUNX2 and aldose reductase regulate glucose-activated endothelial cell wound healing Homo sapiens