2.6.1.64: glutamine-phenylpyruvate transaminase
This is an abbreviated version!
For detailed information about glutamine-phenylpyruvate transaminase, go to the full flat file.
Word Map on EC 2.6.1.64
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2.6.1.64
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pyridoxal
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aminotransferases
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transamination
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asparaginase
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dicarboxylic
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alpha-keto-gamma-methiolbutyric
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3.5.1.1
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2.6.1.51
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selenols
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se-conjugates
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l-kynurenine
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selenocysteine
- 2.6.1.64
- pyridoxal
- aminotransferases
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transamination
- asparaginase
-
dicarboxylic
-
alpha-keto-gamma-methiolbutyric
-
3.5.1.1
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2.6.1.51
-
selenols
-
se-conjugates
- l-kynurenine
- selenocysteine
Reaction
Synonyms
cysteine conjugate beta-lyase/glutamine transaminase K, EC 2.6.1.14, EC 2.6.1.15, EC 2.6.1.7, Gln/phenylpyruvate transaminase, glutamic-oxaloacetic transaminase, glutamine transaminase K, glutamine transaminase L, glutamine transaminase-K, glutamine-phenylpyruvate aminotransferase, glutamine/phenylpyruvate transaminase, GOT1, GTK, histidine pyruvate aminotransferase isoenzyme 2, KAT/GTK, kynurenine aminotransferase/glutamine transaminase K
ECTree
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General Information
General Information on EC 2.6.1.64 - glutamine-phenylpyruvate transaminase
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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