BCAT1 (Branched Chain Amino Acid Transaminase 1 )

P=N/A, N=5000, Recruiting, Flinders University of South Australia | N=3000 --> 5000

DDX6 KO leads to rapid PB dissolution and release of PB-enriched mRNAs, such as BCAT1, into the cytosol, where these transcripts undergo degradation. By reducing BCAT1 levels, DDX6 KO reprograms amino acid metabolism and sensitizes AML cells to cytarabine chemotherapy.

Quantitative analysis of DNA methylation at CpG sites near the C3orf37 gene appears to be a promising approach to distinguish between index and indolent prostate cancer cells.

This study demonstrates the feasibility of applying behavioural science and SDM frameworks to analyse trial recruitment consultations. While a range of BCTs were identified, SDM efforts were generally low. Recruitment practices may benefit from more deliberate consideration of these techniques and greater emphasis on shared decision-making to support informed choices.

While gabapentin (Gp) can inhibit BCAA catabolism by targeting branched-chain amino acid aminotransferase 1 (BCAT1), its efficacy is limited by inefficient delivery and compensatory mitochondrial metabolism...Metabolomic analyses further confirmed synergistic BCAA metabolic inhibition and copper-induced mitochondrial dysfunction. This work presents a promising metabolic intervention strategy for pancreatic cancer through targeted nanomedicine.

This subsequently elevated branched-chain amino acid (BCAA) metabolism in lung cancer cells. Overall, our findings highlight the tumor-promoting role of PTGFRN in non-small cell lung cancer and demonstrate that PTGFRN accelerates cancer progression by enhancing the STAT3/BCAT1 signaling axis and reprogramming BCAA metabolism.

The integration of magnetic resonance elastography, atomic force microscopy, and single-cell sequencing allows detailed research characterization of the biomechanical properties of PDAC. ITGB5 has been identified as an important regulator of the biomechanical features of PDAC. Targeting ITGB5 in CAFs may reduce the excessive stiffness of PDAC tissue and mitigate gemcitabine-associated stromal fibrosis, suggesting a potential strategy to improve treatment response. The effect on patient prognosis, however, requires confirmation in clinical studies.

Evidence from both in vitro and in vivo studies indicated that BCAT1 might foster an immunosuppressive environment by driving M2 macrophage polarization, which could account for the aggressive spread of LUAD and suboptimal responses to immunotherapy. Overall, our findings flagged BCAT1-high-expressing macrophages as a suppressive element in the TME, hinting that targeting BCAT1 could shift macrophage polarization and enhance patient outcomes.

Molecular docking analysis demonstrates that PET can tightly bind to specific target proteins, suggesting a potential molecular mechanism underlying OS progression. These findings provide a scientific basis for further evaluating PET-related health risks and offer theoretical support for the development of future prevention and treatment strategies.

This study identifies GBP4-related prognostic genes and demonstrates the role of GBP4 in pancreatic cancer progression, providing new perspectives for prognostic prediction and therapeutic targeting.

T-independent BCR/TLR9 co-stimulation, which drives malignant and autoimmune B-cell states highly induced the transaminase branched chain amino acid transaminase 1 (BCAT1), which localized to lysosomal membranes to support branched chain amino acid synthesis and mechanistic target of rapamycin complex 1 (mTORC1) activation. BCAT1 inhibition blunted BCR/TLR9, but not CD40L/IL4-triggered B-cell proliferation, IL10 expression and BCR/TLR pathway-driven lymphoma xenograft outgrowth. These results provide a valuable resource, reveal receptor-mediated immunometabolism remodeling to support key B-cell phenotypes and identify BCAT1 as an activated B-cell therapeutic target.

Moreover, the proliferation and invasion status induced by ACSS2 can be partly reversed by BCAT1 in pancreatic cancer cells. In summary, we believe that targeting the ACSS2-PPARD-BCAT1 axis has certain clinical value and can provide a new therapeutic strategy for the comprehensive treatment of pancreatic cancer.