Ask about this productRelated genes to: BCAT1 antibody
- Gene:
- BCAT1 NIH gene
- Name:
- branched chain amino acid transaminase 1
- Previous symbol:
- BCT1
- Synonyms:
- -
- Chromosome:
- 12p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-03-07
Related products to: BCAT1 antibody
Related articles to: BCAT1 antibody
- ObjectiveTo identify metabolism-related genes associated with osteoporosis and evaluate their diagnostic potential through integrative transcriptomic analysis and clinical validation.MethodsSingle-cell RNA sequencing data from GSE169396 were analyzed using the Seurat package to investigate interactions between monocytes and other cell types. Metabolic pathway alterations in osteoporosis were evaluated using single-sample gene set enrichment analysis. Differentially expressed genes were intersected with metabolism-related genes to identify differentially expressed metabolism-related genes. Key metabolic genes were screened using the least absolute shrinkage and selection operator, support vector machine-recursive feature elimination, and Boruta algorithms, and a logistic regression model was established to assess their diagnostic value. External quantitative reverse transcription polymerase chain reaction validation was performed using peripheral blood mononuclear cells from patients with osteoporosis and healthy controls. Receiver operating characteristic curve analysis was used to evaluate the predictive performance of individual genes and the combined model.ResultsSingle-cell interaction analysis revealed close communication between monocyte subsets and hematopoietic stem cells, endothelial cells, cDC2, cDC1, T cells, and plasmacytoid dendritic cells. Significant alterations were observed in valine, leucine, and isoleucine biosynthesis; purine metabolism; fatty acid biosynthesis and elongation; ascorbate and aldarate metabolism; and steroid biosynthesis. Intersection analysis identified 11 differentially expressed metabolism-related genes from 232 metabolism-related genes and 395 differentially expressed genes. Integrative machine learning identified seven key metabolic genes: ADSL, BCAT1, BCAT2, PDE8A, NPR2, SOAT2, and XDH. External validation confirmed significant differential expression of these genes between patients with osteoporosis and healthy controls. The logistic regression model showed excellent diagnostic performance, with an area under the curve of 0.935, whereas all individual genes achieved area under the curve values above 0.7. Gene set enrichment analysis indicated that these genes were enriched in pathways related to G protein-coupled receptor activity.ConclusionsWe identified seven key metabolic genes associated with osteoporosis, namely, ADSL, BCAT1, BCAT2, PDE8A, NPR2, SOAT2, and XDH, and demonstrated their promising diagnostic potential. These findings provide new insights into the metabolic mechanisms underlying osteoporosis and may support the development of future diagnostic biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/09/28
He YunfeiShi CaihongYu XinWang An - This study aims to investigate whether Methyl-Transferase-Like Protein 16 (METTL16) promotes colorectal cancer (CRC) progression through regulating branched-chain amino acid (BCAA) transaminase 1 (BCAT1)-mediated metabolism to modulate CD8T cell-mediated anti-tumor immunity. METTL16 levels were measured in clinical CRC samples and cell models using IHC, qPCR and western blot. Functional assays (CCK-8, EdU, wound healing, transwell) were performed to evaluate the impact of METTL16 knockdown on CRC cell behaviors. A co-culture system with CD8T cells was established to assess immune evasion mechanisms. RIP, MeRIP, and mRNA stability assays were conducted to explore METTL16's regulation of BCAT1 via m6A modification. Metabolomics analysis using LC-MS/MS quantified branched-chain amino acids (BCAAs). In vivo experiments utilized a xenograft mouse model to validate findings. METTL16 was elevated in CRC. Knockdown of METTL16 suppressed malignant phenotype of CRC cell, while enhancing CD8T cell proliferation and cytotoxic molecule secretion (IFN-γ, IL-2, and GzmB). METTL16 regulated BCAT1 expression through m6A-dependent mRNA stabilization, promoting BCAAs metabolism. Rescue experiments demonstrated that BCAT1 overexpression reversed the regulation of METTL16 knockdown on tumor cell malignancy and CD8 T cell responses. In vivo, METTL16 depletion inhibited tumor growth, reduced Ki-67 expression, and enhanced CD8T cell infiltration and effector molecule levels. METTL16 drives CRC progression by promoting BCAT1-mediated BCAAs metabolism and facilitating immune evasion through suppression of CD8T cell function. - Source: PubMed
Publication date: 2026/09/25
Hu YanyanLi ShengyingZhu MinjingLin XuedanGong ChaojuFang Zejun - Cancer-associated fibroblasts (CAFs) are major regulators of the tumor microenvironment, yet how distinct CAF states suppress innate immunity in HER2-low breast cancer remains poorly understood. Here, we identify an S100A4-enriched CAF population that expands during HER2-low breast tumor progression and establishes a metabolically immunosuppressive niche. Spatial transcriptomics and multiplex imaging of human HER2-low tumors reveal progressive CAF accumulation and an inverse spatial association between S100A4-enriched CAFs and immune infiltration, including natural killer (NK) cells. Using an immunocompetent HER2-low mammary tumor model, we show that S100A4-enriched CAFs promote tumor initiation and progression while suppressing NK-cell cytotoxicity, IFN-γ production, perforin, and granzyme B. Fractionation of CAF-conditioned media and metabolic profiling identify a low-molecular-weight immunosuppressive program characterized by enhanced branched-chain amino acid catabolism and accumulation of branched-chain α-keto acids (BCKAs). Mechanistically, BCKAs directly suppress NK-cell IFN-γ production, whereas inhibition of the branched-chain aminotransferase BCAT1 reduces CAF-mediated NK-cell suppression and restores antitumor cytotoxicity. BCAT1 inhibition also suppresses HER2-low tumor growth , an effect attenuated by NK-cell depletion, establishing NK-cell restoration as a functional component of its antitumor activity. Together, these findings uncover a CAF-driven metabolic immune checkpoint in which S100A4-enriched CAFs exploit BCAT1-dependent BCKA production to suppress NK-cell surveillance and promote HER2-low breast tumor progression. Targeting stromal BCAT1 therefore represents a potential strategy to dismantle CAF-mediated immune suppression and restore innate antitumor immunity. - Source: PubMed
Publication date: 2026/09/14
Carter KaylaOgunlusi OlajumokeSarkar MrinmoyAkanbi StephenNguyen ChristianNekkanti ManasaAgarwal AkashFails DanielleNawaratna Gayan IKlemashevich CoryCai JamesBoland Devon JRoy Sarkar Tapasree - Fibrosis remains a major driver of organ dysfunction, yet the metabolic programs that sustain extracellular matrix production are incompletely understood. In this issue of the JCI, Takizawa and colleagues identified branched-chain amino acid transaminase 1 (BCAT1) as a crucial metabolic regulator of fibroblast activation and fibrosis in a model of cardiac fibrosis. Their observations were corroborated by analyses of datasets from patients with heart failure with preserved ejection fraction and metabolic dysfunction-associated steatohepatitis. They report that by coupling mechanical and TGF-β signaling to a proline biosynthesis and utilization program, BCAT1 enhanced collagen production in activated cardiac fibroblasts. These findings place branched-chain amino acid metabolism as a pivotal contributor to fibroblast activation and highlight BCAT1 as a promising therapeutic target for fibrotic disease. - Source: PubMed
Publication date: 2026/09/01
Ronfini MarcoElrod John W - Branched-chain amino acid (BCAA) transaminase 1 (BCAT1), the rate-limiting enzyme in BCAA metabolism, serves a pivotal role in tumor progression. Astragaloside IV (AS-IV) exhibits potential antitumor properties; however, whether AS-IV suppresses breast cancer migration by modulating BCAA metabolism via BCAT1 remains to be elucidated. The present study aimed to investigate whether AS-IV inhibits the invasion and migration of MDA-MB-231 triple-negative breast cancer (TNBC) cells by targeting BCAT1-mediated BCAA metabolic reprogramming. The present study used network pharmacology to predict AS-IV targets against breast cancer invasion, followed by BCAT1 knockdown and overexpression in MDA-MB-231 cells. Using molecular docking, cellular thermal shift assay, wound healing, Transwell, western blotting, quantitative PCR and liquid chromatography-mass spectrometry metabolomics, the present study systematically evaluated: i) AS-IV-BCAT1 direct binding and protein stability; ii) BCAA metabolic flux regulation via the branched-chain α-ketoacid dehydrogenase kinase (BCKDK)/branched-chain α-ketoacid dehydrogenase (BCKDH) axis; and iii) functional impacts on breast cancer cell migration and invasion. Network pharmacology predicted BCAT1 as a key potential target of AS-IV, with significant enrichment of the BCAA metabolic pathway. The results of the present study suggested that AS-IV binds to and stabilizes BCAT1 , an effect that is associated with reduced migration and invasion of MDA-MB-231 cells. It also promotes BCAA degradation via the BCKDK/BCKDH axis, lowering intracellular BCAA levels and suppressing malignancy. Notably, AS-IV maintained dose-dependent inhibition even with BCAT1 knockdown or overexpression, albeit with reduced efficacy. In conclusion, the present study suggested that AS-IV suppresses MDA-MB-231 cell invasion and migration by targeting BCAT1-mediated BCAA metabolism. These findings support further evaluation of AS-IV in TNBC and highlight BCAA metabolism as a potential intervention point in future research. - Source: PubMed
Publication date: 2026/08/03
Liu Yi-TingZhang LuSun Xiao-Dong