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
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1.14.11.16
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prolyl
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hydroxylases
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oxygen-dependent
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ankyrin
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hif-alpha
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oxygen-sensing
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junctin
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humbug
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fih-dependent
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fih-mediated
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alpha-ketoglutarate-dependent
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junctate
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medicine
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analysis
- 1.14.11.16
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prolyl
- hydroxylases
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oxygen-dependent
- ankyrin
-
hif-alpha
-
oxygen-sensing
-
junctin
-
humbug
-
fih-dependent
-
fih-mediated
-
alpha-ketoglutarate-dependent
-
junctate
- medicine
- analysis
Reaction
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
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Source Tissue on EC 1.14.11.16 - peptide-aspartate beta-dioxygenase
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SOURCE TISSUE 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
SOURCE
additional information
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highly expressed in 4 of 10 hepatocarcinomas, 10-fold activity increase
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
additional information
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the enzyme is overexpressed in a wide variety of human malignancies such as breast, hepatic, biliary, colon, pulmonary, pancreatic, and neural origin
additional information
the enzyme is present on the cell surface of invasive cancer cells
