BCAT2 Antibody
- Known as:
- BCAT2 Antibody
- Catalog number:
- csb-pa002601la01hu
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- CusAb
- Gene target:
- BCAT2 Antibody
Related genes to: BCAT2 Antibody
- Gene:
- BCAT2 NIH gene
- Name:
- branched chain amino acid transaminase 2
- Previous symbol:
- BCT2
- Synonyms:
- BCAM
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-03-07
Related products to: BCAT2 Antibody
Related articles to: BCAT2 Antibody
- Lung cancer bone metastasis presents a major clinical challenge due to therapeutic resistance and severe morbidity. Although disrupting tumor-bone microenvironment crosstalk is a promising strategy, clinically actionable targets remain limited. Here, by analyzing bulk RNA sequencing data from bone metastatic tumors across multiple cancer types, we identified PARP10 as a gene consistently upregulated in bone metastases. High PARP10 expression in primary tumors was correlated with poor patient survival. Functional studies demonstrated that PARP10 promoted lung cancer growth and bone metastasis both in vitro and in vivo. Mechanistically, multi-omics integrated analyses revealed that PARP10 deletion induced DNA damage and oxidative stress, and upregulated BCAT2 expression in a MYC-dependent manner to enhance BCAA catabolism. This metabolism exerts an adaptive compensatory effect on tumor cells via boosting mitochondrial oxidative phosphorylation, yet depletes bone microenvironmental BCAA and consequently suppresses osteoclast differentiation, thereby inhibiting bone metastasis. Importantly, pharmacological inhibition of PARP10 with OUL232 mitigated bone metastatic burden in mice without observable toxicity, demonstrating its therapeutic potential by concurrently inducing tumor cell apoptosis and disrupting the pro-metastatic niche. Our findings establish PARP10 as a central regulator of a targetable metabolic competition axis and propose its inhibition as a dual-mechanism strategy that simultaneously attacks tumor cells and disrupts the pro-metastatic niche. - Source: PubMed
Publication date: 2026/06/19
Qin YahanXue KeXu YujianPan HongyuChai WenjunSun LeiLiu XiaoliLi JingCao YueLi JingLiu QianYan Mingxia - Asymptomatic Alzheimer's disease (AsymAD) refers to individuals who, despite exhibiting amyloid-β plaques and tau pathology comparable to Alzheimer's disease (AD), maintain cognitive performance similar to cognitively normal individuals. The resilience mechanism in AsymAD individuals remains understudied. We performed a systematic analysis comparing AsymAD and AD across multiple cohorts (ROSMAP, Banner and Mount Sinai), brain regions (BA6, BA9, BA36 and BA37) and neuronal and glial cell types using proteomics and transcriptomics data. AsymAD brains exhibited preserved mitochondrial bioenergetics, characterized by enhanced oxidative phosphorylation, electron transport chain activity, fatty acid and lipid metabolism, and branched-chain amino acid utilization. Pathways regulating mitochondrial complex biogenesis and calcium homeostasis were also upregulated. Key mitochondrial proteins such as MRPL47, CPT2, BCAT2, and IDH2, were consistently upregulated in AsymAD. At the cellular level, excitatory neurons, including superficial, mid-layer, and deep-layer subtypes, exhibited the most preserved mitochondrial function, whereas vulnerable inhibitory subtypes, including PVALB and SST neurons, showed increased cellular abundance and bioenergetic activity. In contrast, microglia and oligodendrocytes proportions were reduced in AsymAD relative to AD. Our findings identify preserved mitochondrial bioenergetics in AsymAD and suggest that enhancing NADH metabolism via NAD+ precursor-based interventions may potentially help in maintaining cognitive function despite amyloid and tau pathology. - Source: PubMed
Publication date: 2026/06/10
Mandal PurbaTrushina EugeniaArnold MatthiasKaddurah-Daouk RimaBaloni Priyanka - Obesity is a chronic and complex disease defined by excessive deposits of fat that may lead to health damage. Branched-chain amino acids (BCAAs), including valine, leucine, and isoleucine, play a significant role in obesity and metabolic processes. BCAA metabolic disorders are a core feature of obesity and its associated metabolic syndrome, but the specific mechanisms and clinical significance remain highly controversial. This review aims to deeply explore the multifaceted roles of BCAAs in obesity. We first outline the catabolic pathways of BCAAs, summarize the key roles of branched-chain α-keto acids (BCKAs) and 3-hydroxyisobutyric acid (3-HIB) as metabolic intermediates in mediating insulin signaling dysregulation, and analyze how BCAA metabolic disorders drive the progression of obesity and its complications by impairing insulin sensitivity, disrupting lipid homeostasis, and exacerbating chronic inflammation. Additionally, to reconcile the long-standing controversy over whether BCAAs are beneficial or harmful, this review provides new insights. Finally, we summarize potential strategies for targeting BCAA metabolism through dietary modifications, exercise interventions, and drug therapies. This review aims to deepen the understanding of the complex role of BCAAs in obesity and lay a theoretical foundation for precise prevention and strategies targeting metabolic pathway imbalances. BCAAs regulate obesity through pathways that affect insulin sensitivity, lipid metabolism, and inflammatory. Insulin sensitivity is regulated by the activity of the mTORC1 signaling pathway and the functional state of mitochondria. The metabolism of branched-chain amino acids influences lipid synthesis and breakdown by inhibiting BCAT2. Elevated levels of branched-chain amino acids may exacerbate inflammatory through macrophage infiltration and the secretion of pro-inflammatory cytokines. On the right are different intervention measures for regulating BCAA levels, including dietary, exercise and drug interventions. (Note:The symbol "↑" indicates promotion/increase, and "↓" indicates inhibition/decrease.). - Source: PubMed
Publication date: 2026/05/22
Wang DingyeWang XiyuanYang Minlan - Poly (ADP-ribose) polymerase inhibitor (PARPi) resistance poses a significant challenge in prostate cancer (PCa). Although branched-chain amino acid (BCAA) metabolism is implicated in cancer biology, its specific role in PARPi resistance remains unclear. This study aims to investigate how BCAA metabolism contributes to PARPi resistance in PCa. - Source: PubMed
Publication date: 2026/05/11
Mei WangliZhou HangLi WeiyiLiu YongqiangTang ChaozhiWei MengyuZhou ZhenYe BowenNiu HanwenWang WeitianYang KaiqiZhang YueHuang LiqunYu YangWen XiaofeiYe Lin - Pancreatic adenocarcinoma (PAAD) is characterized by profound metabolic reprogramming, including altered branched-chain amino acid (BCAA) metabolism. While the tumor-promoting role of branched-chain aminotransferase 2 (BCAT2) in PAAD has been well documented, the function of branched-chain aminotransferase 1 (BCAT1) remains unclear, particularly in PAAD cells with low endogenous BCAT1 expression. This study aimed to define the context-dependent role of BCAT1 in PAAD and to elucidate the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/05/07
Huang HuiminLiu XinhengChen XiTang XinyiQiu HanxiangYu HuajunJin GuihuaLan Linhua