EC Number |
General Information |
Reference |
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2.6.1.13 | evolution |
ornithine aminotransferase is a highly conserved enzyme present in all prokaryotes and eukaryotes, from unicellular bacteria to multicellular animals and plants. In Triticum aestivum, three homeologous OAT genes in wheat genome are found on chromosome group 5, named as TaOAT-5AL, TaOAT-5BL, and TaOAT-5DL. The phylogenetic tree indicates that OATs share highly conserved domains between monocotyledons and eudicotyledons |
758976 |
2.6.1.13 | evolution |
ornithine aminotransferase is a highly conserved enzyme present in all prokaryotes and eukaryotes, from unicellular bacteria to multicellular animals and plants. In Triticum aestivum, three homeologous OAT genes in wheat genome are found on chromosome group 5, named as TaOAT-5AL, TaOAT-5BL, and TaOAT-5DL. Two transcript variants of TaOAT-5AL are revealed, named TaOAT-5AL-1 and TaOAT-5AL-2 and characterized by 1497 bp and 1287 bp in cDNA length, respectively. Compared to TaOAT-5AL-2, TaOAT-5AL-1 contains an additional 120-bp insertion encompassing an in-frame stop codon, which resulted in a premature protein. The additional insertion is genotypically confirmed by sequencing results from six cultivars. The phylogenetic tree indicates that OATs share highly conserved domains between monocotyledons and eudicotyledons |
758976 |
2.6.1.13 | malfunction |
a deficit in ornithine aminotransferase (OAT) is associated with gyrate atrophy, a rare autosomal recessive disorder causing progressive blindness and chorioretinal degeneration |
760090 |
2.6.1.13 | malfunction |
deltaOAT and proline dehydrogenases (ProDH1 and ProDH2) are involved in the defence against non-host pathogens. Mutants for these genes compromise non-host resistance and show a decrease in non-host pathogen-induced reactive oxygen species |
723382 |
2.6.1.13 | malfunction |
deltaOAT and proline dehydrogenases (ProDH1 and ProDH2) are involved in the defence against non-host pathogens. Silencing of these genes in Nicotina benthamiana delays occurrence of hypersensitive response and favours non-host pathogen growth |
723382 |
2.6.1.13 | malfunction |
mutation of Val79 to Tyr results in a change of substrate preference between GABA, N-acetylornithine and L-ornithine, suggesting a key role of Val79 in defining substrate specificity |
-, 758756 |
2.6.1.13 | malfunction |
overexpression of OAT promotes the growth and metastasis of A-549 lung cancer cells, and overexpression of OAT also promotes the epithelial-mesenchymal transition (EMT) of OAT-overexpressing A549 cells. Knockdown of OAT inhibits the proliferation and metastasis of H-1299 cells |
759545 |
2.6.1.13 | malfunction |
selective inhibition of hOAT has been shown to effectively suppress hepatocellular carcinoma (HCC) tumor growth in vivo |
759413 |
2.6.1.13 | malfunction |
the influence of OAT activity in a model of septic shock induced by intraperitoneal injection of lipopolysaccharide in wild-type and transgenic mice overexpressing OAT in the liver, kidney and intestine is analysed. OAT overexpression has only limited metabolic consequences, most probably because of compensatory mechanisms ensuring amino acid homeostasis. OAT overexpression brings a metabolic advantage in the response to stress. Results show an inhibition of OAT activity and expression in the liver following LPS treatment |
721263 |
2.6.1.13 | malfunction |
the R180T variant of delta-ornithine aminotransferase is associated with gyrate atrophy. Ornithine delta-aminotransferase deficiency is responsible for gyrate atrophy (GA), an autosomal recessive disorder causing a progressive degeneration of the choroid and retina epithelium leading to blindness in young adults |
759181 |