Localization | Comment | Organism | GeneOntology No. | Textmining |
---|---|---|---|---|
mitochondrion | - |
Homo sapiens | 5739 | - |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | Q12797 | - |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
hepatoma cell line | 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 | Homo sapiens | - |
Synonyms | Comment | Organism |
---|---|---|
aspartate beta-hydroxylase | - |
Homo sapiens |
ASPH | - |
Homo sapiens |
Organism | Comment | Expression |
---|---|---|
Homo sapiens | 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 | up |