Protein Variants | Comment | Organism |
---|---|---|
additional information | isozyme BCAT1 knockdown represses the growth rate of MCF-7 and T47D cells since day 2. mitochondrial BCAT1 knockdown reduces mitochondrial DNA content, whereas BCAT1 overexpression increases mitochondrial DNA content in MCF-7 and T47D cells. BCAT1 knockdown represses mTOR signaling, and BCAT1 overexpression activates mTOR signaling | Homo sapiens |
Localization | Comment | Organism | GeneOntology No. | Textmining |
---|---|---|---|---|
mitochondrion | - |
Homo sapiens | 5739 | - |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
L-isoleucine + 2-oxoglutarate | Homo sapiens | - |
3-methyl-2-oxopentanoate + L-glutamate | - |
r | |
L-leucine + 2-oxoglutarate | Homo sapiens | - |
4-methyl-2-oxopentanoate + L-glutamate | - |
r | |
L-valine + 2-oxoglutarate | Homo sapiens | - |
3-methyl-2-oxobutanoate + L-glutamate | - |
r |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | P54687 | - |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
breast cancer cell | - |
Homo sapiens | - |
MCF-7 cell | - |
Homo sapiens | - |
T-47D cell | - |
Homo sapiens | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
L-isoleucine + 2-oxoglutarate | - |
Homo sapiens | 3-methyl-2-oxopentanoate + L-glutamate | - |
r | |
L-leucine + 2-oxoglutarate | - |
Homo sapiens | 4-methyl-2-oxopentanoate + L-glutamate | - |
r | |
L-valine + 2-oxoglutarate | - |
Homo sapiens | 3-methyl-2-oxobutanoate + L-glutamate | - |
r |
Synonyms | Comment | Organism |
---|---|---|
BCAT1 | - |
Homo sapiens |
branched-chain amino acid transaminase 1 | - |
Homo sapiens |
Cofactor | Comment | Organism | Structure |
---|---|---|---|
pyridoxal 5'-phosphate | PLP | Homo sapiens |
General Information | Comment | Organism |
---|---|---|
malfunction | knockdown of BCAT1 represses the growth rate and colony formation capacity of breast cancer cells, opposing results are observed when BCAT1 is overexpressed. BCAT1 can promote mitochondrial biogenesis, ATP production and repress mitochondrial ROS in breast cancer cells by regulating the expression of related genes. BCAA catabolism is activated in human breast cancer, and abolishment of BCAA catabolism by knocking down BCAT1 inhibits breast cancer cell growth by repressing mTOR-mediated mitochondrial biogenesis and function. BCAT1 overexpression is unable to affect the mRNA levels of the genes involved in mitochondrial biogenesis (PGC1alpha, NRF-1, Tfam, and beta-F1-ATPase) and oxidative stress (SOD1, SOD2, catalase, and Gpx1) | Homo sapiens |
metabolism | levels of branched-chain amino acids (BCAAs: leucine, isoleucine, and valine) are significantly upregulated in the serum of patients with breast cancer compared with healthy donors. Also the mRNA levels of BCAT1, BCAT2, mitochondrial targeted 2C-type serine/threonine protein phosphatase (PP2Cm), branched chain keto acid dehydrogenase E1, alpha polypeptide (BCKDHA), BCKDHB, and enoyl-CoA hydratase, short chain 1 (ECHS1) are increased in human breast cancer tissues compared with matched adjacent normal tissues | Homo sapiens |
physiological function | branched-chain amino acids (BCAAs) are important nutrient signals that have direct and indirect effects. BCAA catabolism is a conserved regulator of physiological aging and participates in diverse physiological and pathological processes, including carcinoma development. BCAA catabolism is involved in human breast cancer. The plasma and tissue levels of BCAAs are increased in breast cancer, which is accompanied by the elevated expression of the catabolic enzymes, including branched-chain amino acid transaminase 1 (BCAT1). BCAT1 promotes the growth of breast cancer cells through improving mTOR-mediated mitochondrial biogenesis and function. BCAT1 activates the mTOR, but not AMPK or SIRT1, signaling to promote mitochondrial biogenesis and function, and subsequently facilitates growth and colony formation of breast cancer cells. BCAA catabolism is activated in human breast cancer. Isozyme BCAT1 promotes growth and colony formation of breast cancer cells | Homo sapiens |