BCAT1 antibody (clone AT3C8)
- Known as:
- BCAT1 (anti-) (clonality AT3C8)
- Catalog number:
- ATGA0359
- Product Quantity:
- 50ul
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- BCAT1 antibody (clone AT3C8)
Related genes to: BCAT1 antibody (clone AT3C8)
- 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 (clone AT3C8)
Related articles to: BCAT1 antibody (clone AT3C8)
- Head and neck squamous cell carcinoma (HNSCC) poses a significant global health challenge, characterized by low survival rates and frequent metastasis. Conventional therapies are often restricted by systemic toxicity and drug resistance, positioning natural bioactive extracts like Total Glucosides of Paeony (TGP) as promising therapeutic alternatives. While the amino acid transporter SLC7A5 is known to drive tumor proliferation by facilitating leucine uptake and activating the mTOR signaling pathway, the specific interaction between TGP and this SLC7A5/mTOR axis in HNSCC has not been fully elucidated. - Source: PubMed
Publication date: 2026/07/11
Li YuanqiangHu GaofengNiu WenyuanZhang LizhuoGe JiamingXuan JieYu XuefeiMa ShangLi MengjiaZhang ZiqiangLuo KeJia XingLi Qinglin - To evaluate the diagnostic performance and clinicopathologic relevance of a multi-locus circulating tumor DNA methylation assay, in this prospective, single-center, case-control exploratory study, we enrolled 35 patients with colorectal cancer undergoing surgery and 57 healthy controls undergoing screening colonoscopy at the Asan Medical Center, Seoul, Republic of Korea between July 2024 and January 2025. Peripheral blood was collected before surgery or colonoscopy, and circulating tumor DNA methylation was analyzed using a multi-locus panel targeting Septin9, IKZF1, BCAT1, Septin9-2, BCAN, and VAV3. The main outcomes were test accuracy (sensitivity, specificity, and area under the curve [AUC]) and associations between methylation marker positivity and clinicopathologic features. Circulating tumor DNA was positive in 74.3% of the patients and 12.3% of controls, yielding a sensitivity of 74.3%, specificity of 87.7%, and an AUC of 0.837, whereas serum carcinoembryonic antigen exhibited lower sensitivity (25.7%). Sensitivity in stage I disease was limited (36.4%). Circulating tumor DNA-positive tumors were larger (5.7 cm vs. 2.2 cm, < 0.001) and had more advanced T and N stages. The number of positive markers increased with pathologic stage ( = 0.003). Individual marker analysis revealed that BCAT1, Septin9-2, and VAV3 were associated with higher T stage, whereas BCAN positivity was linked to nodal metastasis. The six-marker circulating tumor DNA methylation assay demonstrated acceptable diagnostic accuracy, with multi-locus patterns associated with tumor burden and invasive features. However, sensitivity for early-stage disease was limited. The assay may serve as a complementary tool for screening and risk stratification. - Source: PubMed
Publication date: 2026/06/25
Lee HayoungKang Jae CheolPark In JaKim Gwang-UnHyun HwiMin Na YoungJeon SungwonKim Byoung-Chul - Brain metastasis (BM) in non-small cell lung cancer (NSCLC) is associated with the reprogramming of branched-chain amino acid (BCAA) metabolism. This investigation sought to comprehend the function and molecular process of BCAT1 during the BM associated with NSCLC. - Source: PubMed
Publication date: 2026/06/25
Yang FanLi YuyingZhou HuijiaoBi XinWang Dongjie - Triple-negative breast cancer (TNBC) lacks effective molecularly targeted therapies. Here, we identify branched-chain amino acid (BCAA) metabolism as a selective vulnerability in human TNBC, particularly in the claudin-low subtype. TNBC cells show greater dependence on BCAAs than other breast cancer subtypes, and intracellular BCAA levels are heterogeneous within tumors in vivo. Cells with high BCAA levels exhibit enhanced sphere formation and cancer stem cell potential in xenograft models. BCAT1, a cytoplasmic BCAA aminotransferase, is upregulated in claudin-low TNBC and enables tumor growth by promoting BCAA production from branched-chain ketoacids. BCAT1 knockdown impairs TNBC growth in vivo, and high BCAT1 expression predicts poor prognosis in patient cohorts. Conversely, BCAA catabolism via the BCKDH complex is suppressed in TNBC, and reactivation of BCKDH by BCKDK knockout blocks clonogenic growth. These findings reveal BCAA metabolic balance as a key regulator of TNBC stemness and malignancy. - Source: PubMed
Publication date: 2026/07/08
Matsuura KenkyoShinonaga RirikoYamamoto MizukiYamamoto YoshikiChen HsinMaeno AyakaOkuda KayoInoue HarukiImotani SotaGlushka JohnMiki KojiWatanabe YukakoTakada MamoruKaji HironoriInoue Jun-IchiroHattori AyunaImamura HiromiIto Takahiro - Metabolic syndrome (MetS) has been associated with increased acute pancreatitis (AP) severity. This study aimed to identify shared differentially expressed genes (CDEGs) between MetS and AP and to prioritize mechanistically relevant targets. The shared genetic basis and causal effect of MetS on AP were first assessed using linkage disequilibrium score regression (LDSC) and two-sample Mendelian randomization (MR). Public Gene Expression Omnibus (GEO) datasets were analyzed to define shared CDEGs. A multi-step pipeline incorporating functional enrichment, protein-protein interaction (PPI) analysis, and transcription factor mapping was used to identify AP hub genes (AP-HGs). Functional relatedness and putative causal relationships were evaluated using GeneMANIA, MR, and single-cell RNA sequencing (scRNA-seq). Finally, computational drug prediction and molecular docking were performed to identify potential therapeutic agents. Key findings were further validated in a hyperlipidemia AP (HAP) model. A positive genetic correlation between MetS and AP was identified by LDSC, and MR supported a causal effect of MetS on increased AP risk. BCAT1, GPAT3, ANP32C, and ZNF683 were identified as CDEGs between MetS and AP. MAPK14 was identified as a central AP-HG. MAPK14, BCAT1, and GPAT3 were effective predictors for severe AP (SAP), with AUCs of 0.738, 0.722, and 0.744, respectively. GeneMANIA predicted a high degree of physical interaction (77.6%) among these genes. MR analysis provided supportive genetic evidence linking MAPK14 expression to inflammatory mediators including IL-1ra and TNFR-1. scRNA-seq analysis in an experimental AP model localized Mapk14 expression predominantly to macrophages, while Bcat1 marked a unique, proliferative fibroblast subpopulation that emerged transiently during inflammation and exhibited an anabolic metabolic signature. Ozagrel was prioritized as an exploratory candidate with favorable predicted binding affinities and requires further validation. In a HAP model, aggravated pancreatic injury and upregulation of BCAT1 and MAPK14 were confirmed under the high-fat background. A genetic and transcriptomic link between MetS and AP was identified. MAPK14-associated inflammation and Bcat1-positive fibroblast remodeling may contribute to AP aggravation under metabolic disturbance. These findings provide candidate biomarkers for SAP prediction and support BCAT1 and MAPK14 as potential mechanistic targets. - Source: PubMed
Zhou XiaoyingYang ChenZou TongxinBasharat ZarrinZippi MaddalenaFiorino SirioHong Wandong