BCAT1 monoclonal antibody (M02), clone 1F8
- Known as:
- BCAT1 mab (anti-) (M02), clonality 1F8
- Catalog number:
- H00000586-M02
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- BCAT1 monoclonal antibody (M02) clone 1F8
Related genes to: BCAT1 monoclonal antibody (M02), clone 1F8
- 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
- Gene:
- EMC10 NIH gene
- Name:
- ER membrane protein complex subunit 10
- Previous symbol:
- C19orf63
- Synonyms:
- INM02, HSS1, HSM1
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2007-07-17
- Date modifiied:
- 2016-12-01
- Gene:
- MRPL1 NIH gene
- Name:
- mitochondrial ribosomal protein L1
- Previous symbol:
- -
- Synonyms:
- BM022
- Chromosome:
- 4q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-02-28
- Date modifiied:
- 2015-08-25
- Gene:
- PMS2 NIH gene
- Name:
- PMS1 homolog 2, mismatch repair system component
- Previous symbol:
- PMSL2
- Synonyms:
- H_DJ0042M02.9, HNPCC4, MLH4
- Chromosome:
- 7p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-13
- Date modifiied:
- 2019-04-23
- Gene:
- SESN2 NIH gene
- Name:
- sestrin 2
- Previous symbol:
- -
- Synonyms:
- SES2, DKFZp761M0212, HI95, SEST2
- Chromosome:
- 1p35.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-03
- Date modifiied:
- 2016-10-05
Related products to: BCAT1 monoclonal antibody (M02), clone 1F8
Related articles to: BCAT1 monoclonal antibody (M02), clone 1F8
- 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 - Asthma is a chronic inflammatory respiratory disease worldwide. Its severe phenotypes, particularly the glucocorticoid-resistant ones, pose a major challenge, with neutrophilic inflammation being the key driver. However, no effective treatments are currently available. Herein, we report a macromolecular therapeutic strategy capable of targeting multiple key cells involved in the pathogenesis of neutrophilic asthma. The macromolecular therapy named PMART is constructed by conjugating artesunate and polyethylene glycol to the triazine scaffold. It is highly water-soluble and can self-assemble into nanomicelles, which enables efficient targeting to inflamed lung tissues and localization in inflammatory cells. In a murine model of neutrophilic asthma, PMART has proven to have in vivo efficacy equivalent to or greater than that of two clinically used anti-asthma drugs. Mechanistically, PMART reduces succinate levels by inhibiting branched-chain amino acid transaminase 1 (BCAT1) overexpression, thereby suppressing neutrophilic inflammation via blocking the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome and the production of pro-inflammatory cytokines. Notably, PMART exhibits a favorable safety profile in mice. Taken together, these data support the potential of PMART as a novel and highly effective therapeutic agent for neutrophilic asthma and other neutrophil-mediated diseases. - Source: PubMed
Publication date: 2026/07/03
Gong JingZhou MinHuang YueYu MengjunZhou QiangChen ShiwenWang JiaYang MinLuo QingZhang RongHuang Jingbin - Gastric cancer (GC) remains a leading cause of cancer-related mortality worldwide, and the prognosis of advanced GC remains poor. Systematic identification of robust biomarkers through multi-cohort integration and computational prioritization may facilitate the discovery of novel therapeutic targets. - Source: PubMed
Publication date: 2026/06/27
Li XinChen JiahanTian HongpenZhang Guangjun - Emerging evidence from correlative and preclinical studies suggest that cancer stem cells (CSCs) may contribute to immunotherapy resistance, in part by remodeling the tumor microenvironment (TME). This review synthesizes findings from spatial transcriptomics, single‑cell analyses, patient‑derived models, and in vivo validation, highlighting mechanisms that have been implicated in CSC‑mediated immune evasion. We map each mechanism to its therapeutic status: intrinsic checkpoints (PD‑L1, CD47, SIGLEC15) → targetable by checkpoint or phagocytosis blockade; extrinsic niche remodeling (SPP1 + macrophages, MDSCs) → targetable by anti‑SPP1 or CSF1R inhibitors; metabolic suppression (lactate, adenosine) → targetable by CD73/IDO1 inhibitors; cellular plasticity (Wnt/β‑catenin, IFNγ/BCAT1) → targetable by Wnt or BCAT1 inhibitors; spatial immune exclusion - no direct therapy currently available, though niche reprogramming may indirectly alleviate it. For many of these pathways, direct causal evidence in patients remains limited. Translational strategies under early investigation include direct CSC targeting (e.g., BCAT1 or Wnt inhibitors), niche reprogramming (e.g., anti‑SPP1, CSF1R inhibitors), and combination with immune checkpoint blockade. Emerging technologies such as CSC‑targeted nanoparticles and engineered cellular therapies are also discussed as hypothesis‑generating approaches. We conclude that while current data are promising, rigorous, biomarker‑driven trials are needed to determine whether targeting the CSC‑associated niche can durably improve anti‑tumor immunity in tumors where CSC-mediated immune evasion predominates. - Source: PubMed
Publication date: 2026/06/23
Abdu Salah AmeenZeng JianAsaad Wafa AliNing Li