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Literature summary extracted from

  • Yang, C.; Stampouloglou, E.; Kingston, N.; Zhang, L.; Monti, S.; Varelas, X.
    Glutamine-utilizing transaminases are a metabolic vulnerability of TAZ/YAP-activated cancer cells (2018), EMBO Rep., 19, e43577 .
    View publication on PubMedView publication on EuropePMC

Cloned(Commentary)

EC Number Cloned (Comment) Organism
2.6.1.52 quantitative real-time PCR enzyme expression analysis Homo sapiens
2.6.1.64 quantitative real-time PCR enzyme expression analysis Homo sapiens

Inhibitors

EC Number Inhibitors Comment Organism Structure
2.6.1.52 Aminooxyacetate AOA, the transaminase inhibitor represses cell growth in a TAZ/YAP-dependent manner Homo sapiens
2.6.1.64 Aminooxyacetate AOA, the transaminase inhibitor represses cell growth in a TAZ/YAP-dependent manner Homo sapiens

Natural Substrates/ Products (Substrates)

EC Number Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
2.6.1.52 O-phospho-L-serine + 2-oxoglutarate Homo sapiens
-
 3-phosphooxypyruvate + L-glutamate
-
 r
2.6.1.64 L-glutamine + phenylpyruvate Homo sapiens
-
 2-oxoglutaramate + L-phenylalanine
-
 ?

Organism

EC Number Organism UniProt Comment Textmining
2.6.1.52 Homo sapiens Q9Y617
-
-
2.6.1.64 Homo sapiens P17174
-
-

Purification (Commentary)

EC Number Purification (Comment) Organism
2.6.1.52 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
2.6.1.64 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

EC Number Source Tissue Comment Organism Textmining
2.6.1.52 breast cancer cell transcriptional regulators TAZ/YAP activity positively correlates with transaminase expression in breast cancer patients Homo sapiens
-
2.6.1.52 BT-474 cell
-
 Homo sapiens
-
2.6.1.52 HCC-38 cell
-
 Homo sapiens
-
2.6.1.52 HMT-3522 S1 cell
-
 Homo sapiens
-
2.6.1.52 MDA-MB-231 cell
-
 Homo sapiens
-
2.6.1.64 breast cancer cell transcriptional regulators TAZ/YAP activity positively correlates with transaminase expression in breast cancer patients Homo sapiens
-
2.6.1.64 BT-474 cell
-
 Homo sapiens
-
2.6.1.64 HCC-38 cell
-
 Homo sapiens
-
2.6.1.64 HMT-3522 S1 cell
-
 Homo sapiens
-
2.6.1.64 MDA-MB-231 cell
-
 Homo sapiens
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
2.6.1.52 O-phospho-L-serine + 2-oxoglutarate
-
 Homo sapiens 3-phosphooxypyruvate + L-glutamate
-
 r
2.6.1.64 L-glutamine + phenylpyruvate
-
 Homo sapiens 2-oxoglutaramate + L-phenylalanine
-
 ?

Synonyms

EC Number Synonyms Comment Organism
2.6.1.52 phosphoserine aminotransferase
-
 Homo sapiens
2.6.1.52 PSAT1
-
 Homo sapiens
2.6.1.64 glutamic-oxaloacetic transaminase
-
 Homo sapiens
2.6.1.64 GOT1
-
 Homo sapiens

Temperature Optimum [°C]

EC Number Temperature Optimum [°C] Temperature Optimum Maximum [°C] Comment Organism
2.6.1.52 37
-
 assay at Homo sapiens
2.6.1.64 37
-
 assay at Homo sapiens

pH Optimum

EC Number pH Optimum Minimum pH Optimum Maximum Comment Organism
2.6.1.52 8.5
-
 assay at Homo sapiens
2.6.1.64 8.5
-
 assay at Homo sapiens

Cofactor

EC Number Cofactor Comment Organism Structure
2.6.1.52 pyridoxal 5'-phosphate
-
 Homo sapiens
2.6.1.64 pyridoxal 5'-phosphate
-
 Homo sapiens

Expression

EC Number Organism Comment Expression
2.6.1.52 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
2.6.1.52 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
2.6.1.64 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
2.6.1.64 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

EC Number General Information Comment Organism
2.6.1.52 metabolism 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 and YAP induce glutamic-oxaloacetic transaminase (GOT1, EC 2.6.1.64) and phosphoserine aminotransferase (PSAT1) 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 Homo sapiens
2.6.1.64 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