Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Automated transfer of experimentally-verified manual GO annotation data to mouse-rat orthologs
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Electronic Gene Ontology annotations created by ARBA machine learning models
Automated transfer of experimentally-verified manual GO annotation data to mouse-human orthologs
Combined Automated Annotation using Multiple IEA Methods
Integrated analysis of protein composition, tissue diversity, and gene regulation in mouse mitochondria.
ENU mutagenesis identifies mice with mitochondrial branched-chain aminotransferase deficiency resembling human maple syrup urine disease.
Disruption of BCATm in mice leads to increased energy expenditure associated with the activation of a futile protein turnover cycle.
A mitochondrial protein compendium elucidates complex I disease biology.
Alcohol-induced IGF-I resistance is ameliorated in mice deficient for mitochondrial branched-chain aminotransferase.
miRNA 34a, 100, and 137 modulate differentiation of mouse embryonic stem cells.
BCAA-BCKA axis regulates WAT browning through acetylation of PRDM16.
Metabolon formation regulates branched-chain amino acid oxidation and homeostasis.
BCAT2-mediated BCAA catabolism is critical for development of pancreatic ductal adenocarcinoma.
Disruption of BCAA metabolism in mice impairs exercise metabolism and endurance.
Cloning of the rat and human mitochondrial branched chain aminotransferases (BCATm).
UniProt entry O35855 (BCAT2_MOUSE)
Liver BCATm transgenic mouse model reveals the important role of the liver in maintaining BCAA homeostasis.
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BCATm is not normally expressed in rodent liver hepatocytes.
"On the other hand, BCATm is not normally expressed in rodent liver or primate hepatocytes."