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1.14.11.16: peptide-aspartate beta-dioxygenase

This is an abbreviated version!
For detailed information about peptide-aspartate beta-dioxygenase, go to the full flat file.

Word Map on EC 1.14.11.16

Reaction

peptide-L-aspartate
+
2-oxoglutarate
 +
O2
=
peptide-3-hydroxy-L-aspartate
 +
succinate
 +
CO2

Synonyms

AAH, asparaginyl hydroxylase factor inhibiting HIF-1, aspartate beta-hydroxylase, aspartate-beta-hydroxylase, aspartate/asparagine-beta-hydroxylase, aspartyl (asparaginyl) beta-hydroxylase, aspartyl (asparaginyl)-beta-hydroxylase, aspartyl beta-hydroxylase, aspartyl-(asparaginyl) beta-hydroxylase, aspartyl-(asparaginyl)-b-hydroxylase, aspartyl-(asparaginyl)-beta-hydroxylase, aspartyl-(asparagyl)-beta-hydroxylase, aspartyl-asparaginyl-beta-hydroxylase, aspartyl/asparaginyl beta-hydroxylase, aspartylpeptide beta-dioxygenase, ASPH, EGF beta-hydroxylase, EGFH, factor inhibiting HIF, factor inhibiting hypoxia-inducible factor, factor inhibiting hypoxia-inducible transcription factor (HIF), factor-inhibiting hypoxia-inducible factor, FIH, HAAH, HIF asparaginyl hydroxylase, human aspartyl (asparaginyl) beta-hydroxylase, hypoxia-inducible factor asparaginyl hydroxylase

ECTree

     1 Oxidoreductases
         1.14 Acting on paired donors, with incorporation or reduction of molecular oxygen
             1.14.11 With 2-oxoglutarate as one donor, and incorporation of one atom of oxygen into each donor
                1.14.11.16 peptide-aspartate beta-dioxygenase

Expression

Expression on EC 1.14.11.16 - peptide-aspartate beta-dioxygenase

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EXPRESSION
ORGANISM
UNIPROT
LITERATURE
about 2fold increase in expression in double transgenic mice with expression of hepatitis Bx and insulin receptor substrate-1 under a liver-specific promoter
-
downregulation of asparaginyl hydroxylase factor inhibiting (FIH) in hepatocellular carcinoma is associated with more aggressive tumor behavior and a poor prognosis
ethanol-treated cultures
-
expression in tumor cells is increased with the development and progression of carcinomas
IGF-1 stimulation increases asparaginyl-beta-hydroxylase protein expression and shifts localization of asparaginyl-beta-hydroxylase from the perinuclear zone to the cell periphery, including podocytes. Subsequently, Notch-1 intracellular domain is translocated to the nucleus, which is critical for Notch-modulated gene expression. Besides glycogen synthase kinase-3beta, inhibition of protein kinase C, protein kinase A, and casein kinase 2, which can potentially phosphorylate asparaginyl-beta-hydroxylase, increases IGF-1 stimulated asparaginyl-beta-hydroxylase protein. Insulin and LiCl independently and additively increase long-term asparaginyl-beta-hydroxylase protein expression
increase after inhibition of GSK-3beta or global caspases
-
increased expression of aspartate beta-hydroxylase in hepatocellular carcinoma tissues is associated with tumor invasiveness and a worse prognosis. Aspartate beta-hydroxylase overexpression in hepatocellular carcinoma tissues is correlated with decreased copy numbers of displacement loop (D-loop) and NADH dehydrogenase subunit 1 and enhanced D-loop mutation, suggesting the disrupted mitochondrial DNA (mtDNA) stability. The reduced mtDNA copy numbers are associated with aggressive clinicopathological features of hepatocellular carcinoma. The loss of mtDNA integrity induced by enforced expression of Aspartate beta-hydroxylase is accompanied with mitochondrial dysfunction, which is characterized by the aberrant mitochondrial membrane potential, decreased ATP generation and enhanced reactive oxygen species. The enzyme interacts with histone H2A member X. Overexpression of aspartate beta-hydroxylase diminishes the interaction between histone H2A member X and mitochondrial transcription factor A (mtTFA), an important DNA-binding protein for mtDNA replication, which then reduced the binding of mtTFA to D-loop region. Overexpression of aspartate beta-hydroxylase disrupts the mtDNA integrity through H2AX-mtTFA signal, thereby affecting mitochondrial functions in hepatocellular carcinoma
overexpressed in breast cancer and correlates with cancer type, lymph node involvement, and TNM stage. The enzyme levels does not correlate with patient age, invasive carcinoma types, or molecular subtypes
overexpression in malignant neoplasms
-
overexpression in many types of cancer tissues
the enzyme is highly overexpressed in pancreatic cancer. Upregulation of the enzyme confers a malignant phenotype characterized by enhanced cell proliferation, migration, invasion and colony formation in vitro as well as pancreatic cancer tumor growth in vivo. The transforming properties of aspartate beta-hydroxylase depend on enzymatic activity
the enzyme is overexpressed in hepatocellular carcinoma and promotes a malignant phenotype
upregulated on the cell surface of invasive cancer cells