Cloned (Comment) | Organism |
---|---|
quantitative real-time PCR enzyme expression analysis | Homo sapiens |
Inhibitors | Comment | Organism | Structure |
---|---|---|---|
Aminooxyacetate | AOA, the transaminase inhibitor represses cell growth in a TAZ/YAP-dependent manner | Homo sapiens |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
L-glutamine + phenylpyruvate | Homo sapiens | - |
2-oxoglutaramate + L-phenylalanine | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | P17174 | - |
- |
Purification (Comment) | Organism |
---|---|
native enzyme from rat brain by ultracentrifugation at 220000 x g, followed by ammonium sulfate fractionation, hydropbobic interaction chromatography, anion exchange chromatography, and hydroxyapatite chromatography | Homo sapiens |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
breast cancer cell | transcriptional regulators TAZ/YAP activity positively correlates with transaminase expression in breast cancer patients | Homo sapiens | - |
BT-474 cell | - |
Homo sapiens | - |
HCC-38 cell | - |
Homo sapiens | - |
HMT-3522 S1 cell | - |
Homo sapiens | - |
MDA-MB-231 cell | - |
Homo sapiens | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
L-glutamine + phenylpyruvate | - |
Homo sapiens | 2-oxoglutaramate + L-phenylalanine | - |
? |
Synonyms | Comment | Organism |
---|---|---|
glutamic-oxaloacetic transaminase | - |
Homo sapiens |
GOT1 | - |
Homo sapiens |
Temperature Optimum [°C] | Temperature Optimum Maximum [°C] | Comment | Organism |
---|---|---|---|
37 | - |
assay at | Homo sapiens |
pH Optimum Minimum | pH Optimum Maximum | Comment | Organism |
---|---|---|---|
8.5 | - |
assay at | Homo sapiens |
Cofactor | Comment | Organism | Structure |
---|---|---|---|
pyridoxal 5'-phosphate | - |
Homo sapiens |
Organism | Comment | Expression |
---|---|---|
Homo sapiens | GOT1 expression level is reduced in TAZ/YAP siRNA knockout cells. The inhibition of transamination preferentially suppresses those breast cancer cells that express high levels of TAZ/YAP (e.g. MDA-MB-231 and HCC38 cells ), not TAZ/YAP-low-level expressing cell lines (e.g. BT474 and HMT-3522 S1) | down |
Homo sapiens | transcriptional regulators TAZ and YAP (TAZ/YAP) promote glutamine dependence in breast cancer cells and activate the expression of glutamine-utilizing transaminases to support cell growth. TAZ/YAP induce glutamic-oxaloacetic transaminase (GOT1) and phosphoserine aminotransferase (PSAT1) expression. TAZ and YAP are required for glutamine-utilizing transaminase expression in breast cancer cells | up |
General Information | Comment | Organism |
---|---|---|
metabolism | glutamine-utilizing transaminases are a metabolic vulnerability of TAZ/YAP-activated cancer cells. Transcriptional regulators TAZ and YAP (TAZ/YAP) promote glutamine dependence in breast cancer cells and activate the expression of glutamine-utilizing transaminases to support cell growth. TAZ/YAP induce glutamic-oxaloacetic transaminase (GOT1) and phosphoserine aminotransferase (PSAT1, EC 2.6.1.52) expression. Transcriptional regulators TAZ/YAP activity positively correlates with transaminase expression in breast cancer patients, while transaminase inhibitor aminooxyacetate (AOA) represses cell growth in a TAZ/YAP-dependent manner. Thus, transamination is a potential vulnerable metabolic requirement for TAZ/YAP-driven breast cancer. TAZ/YAP promote anaplerotic entry of glutamine through transamination | Homo sapiens |