anti-Branched Chain Amino-Acid Transaminase 1, Cytosolic (BCAT1) Antibodies

Human Branched Chain Amino-Acid Transaminase 1, Cytosolic (BCAT1) interaction partners

1. regulatory role in macrophage function

2. Data suggest that both oncogenic mutations and cancer tissue-of-origin influence BCAA (branched-chain amino acid) metabolism in neoplastic tissue and neoplastic expression of cytosolic BCAT1 and mitochondrial BCAT2. (BCAT = branched-chain-amino-acid transaminase) [REVIEW]

3. by limiting intracellular alphaKG, BCAT1 links branched-chain amino acid catabolism to HIF1alpha stability and regulation of the epigenomic landscape, mimicking the effects of IDH mutations; results suggest the BCAA-BCAT1-alphaKG pathway as a therapeutic target to compromise leukaemia stem-cell function in patients with IDH(WT)TET2(WT) AML

4. BCAT1 plays a pathogenic role in hepatocellular carcinoma (HCC) by causing cell proliferation and chemoresistance. The MYC transcription factor is involved in regulating the transcriptional activity of BCAT1. BCAT1 expression has prognostic significance for the survival of patients with HCC.

5. Phenotypic analyses using a lentiviral-mediated BCAT1 short hairpin RNA knockdown revealed that BCAT1 sustains proliferation in addition to migration and invasion and that its overexpression enhanced the capacity of antiestrogen-sensitive cells to grow in the presence of antiestrogens.

6. The tumor suppressive role of miR-218 was mediated by negatively regulating branched-chain amino acid transaminase 1 (BCAT1) protein expression. Importantly, overexpression of BCAT1 decreased the chemosensitivity to cis-diaminedichloroplatinum treatment of PC3 and DU145 cells.

7. It has been demonstrated that branched-chain amino acid (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.

8. BCAT1 expression is significantly upregulated in human masticatory mucosa during wound healing

9. Mechanistic investigation revealed that BCAT1 might be an important regulator responsible for DOT1L-mediated sphere formation and cell migration in breast cancer cells

10. BCAT1 overexpression is associated with advanced tumour status, and implies adverse clinical outcomes of urothelial carcinoma

11. BCAT1 is strongly overexpressed in ovarian cancer.

12. Focal deletions of the BCAT1 were associated with B-cell precursor acute lymphoblastic leukemia.

13. levels of branched-chain aminotransferase-1 (BCAT1) transcripts are significantly decreased on the polysomes of both RPS19 and RPL11 cells and that translation of BCAT1 protein is especially impaired in cells with small RP gene mutations

14. Over-expression of BCAT1, a c-Myc target gene, induces cell proliferation, migration and invasion in nasopharyngeal carcinoma.

15. A central role for BCAT1 in glioma pathogenesis, making BCAT1 and branched-chain amino acids metabolism attractive targets for the development of targeted therapeutic approaches to treat patients with glioblastoma.

16. The mitochondrial isoform human brain BCAT 2 is largely confined to vascular endothelial cells, whereas the cytosolic human brain BCAT 1 is restricted to neurons.

17. BCATc (cytosolic) has an overall redox potential that is 30 mV lower than BCATm (mitochondrial). Furthermore, the CXXC motif of BCATc was estimated to be 80 mV lower, suggesting that BCATm is more oxidizing in nature.

18. Our results suggest that ECA39 is a dominant predictive factor for distant metastasis in patients with advanced colorectal cancer (CRC).

19. The BCAT1 identified in the amplified 12p11-p12 region may play a certain role in nasopharyngeal carcinoma development.

20. hBCATc has redox mediated associations with several neuronal proteins involved in G-protein cell signaling, indicating a novel role for hBCATc in cellular redox control

Mouse (Murine) Branched Chain Amino-Acid Transaminase 1, Cytosolic (BCAT1) interaction partners

1. regulatory role in macrophage function

2. results suggest transcriptional adaptations occur in BCATm KO mice that along with altered nutrient signaling may contribute to their previously reported protein turnover, metabolic and exercise phenotypes

3. BCATc as a novel regulator of T cell activation and metabolism

4. leucine supplementation increased the expression of enzymes (BCAT1, BCAT2 and BCKDK) that metabolize branched-chain amino acids.

5. analysis of the biochemical mechanism of BCATm (branched-chain aminotransferase) catalysis of reversible transamination of leucine and alpha-ketoglutarate to KIC and glutamate

6. Bcat1 is a candidate for the type I diabetes susceptibility locus Idd6

7. Bcat1 is part of the complex multigenic Pas1 locus, with a functional role for its intragenic polymorphisms in lung tumor susceptibility.

8. These results demonstrate that the expression of the BCATc gene in the brain is specifically regulated by BDNF in a time- and region-dependent fashion.

9. BCATc mRNA gradually appears in different brain regions starting from early stages of neural development, and is maintained until adulthood.

10. BCATm(-/-) mice had elevated plasma branched-chain amino acids & decreased adiposity & body weight, despite eating more food, along with increased energy expenditure, improvements in glucose & insulin tolerance & protection from diet-induced obesity