BCKDK ELISA kit
- Known as:
- BCKDK Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-BCKDK-Ra
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- BCKDK ELISA kit
Related genes to: BCKDK ELISA kit
- Gene:
- BCKDK NIH gene
- Name:
- branched chain ketoacid dehydrogenase kinase
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-20
- Date modifiied:
- 2014-11-18
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- Pulmonary fibrosis (PF) is a life-threatening disease characterized by progressive dyspnea and worsening pulmonary function. Branched-chain amino acids (BCAAs) are a group of essential amino acids consisting of valine, leucine, and isoleucine. BCAAs can be converted into intermediate products, branched-chain α-keto acids (BCKAs), which undergo irreversible decarboxylation and dehydrogenation reactions under the action of the branched-chain α-keto acid dehydrogenase complex (BCKDH). Although evidence suggests that the deficiency of BCAA catabolism contributes to tumor and heart failure, the contribution of BCAA metabolism regulation to PF remains largely elusive. - Source: PubMed
Publication date: 2026/05/07
Xiong Da-YanZhang Chen-YuZhang Yan-FengZeng QianLiu WeiYang Nan-Shi-YuTang Si-YuanZheng Jia-HuiZhou YongHuang Xiao-Ting - Metabolic diseases such as obesity, type 2 diabetes mellitus (T2DM), dyslipidaemia, and metabolic dysfunction-associated steatotic liver disease (MASLD) are increasingly recognised as chronic inflammatory conditions driven in part by innate immune dysregulation. Among the metabolic factors implicated in this process, branched-chain amino acids (BCAAs) have emerged as key regulators linking nutrient sensing to immune cell function. Circulating BCAA concentrations are consistently elevated in these metabolic diseases. However, experimental and clinical studies also show that BCAA supplementation can improve metabolic and immune outcomes in specific contexts, revealing a paradoxical relationship between BCAA metabolism and inflammation. This narrative review examines how dysregulated BCAA metabolism and accumulation of branched-chain keto acids (BCKAs) shape the functional programming of innate immune cells across these conditions, including monocytes/macrophages, granulocytes, dendritic cells, and natural killer cells. Evidence indicates that the immunometabolic effects of BCAAs depend not solely on circulating concentrations but on the efficiency of their intracellular catabolism. When BCAA oxidation is preserved, these amino acids support mitochondrial metabolism and immune competence. Conversely, impaired catabolism leads to the accumulation of branched chain ketoacids, which activate inflammatory pathways and contribute to metabolic dysfunction. Resolving this paradox requires the need of targeting catabolic flux restoration rather than simple BCAA restriction or supplementation, and requires stratifying patients by enzymatic capacity, BCAA/BCKA ratios, and disease stage. Pharmacological modulators, including BCKDK inhibitors and BCAT1-targeted agents, show promise in simultaneously addressing metabolic and immune dysregulation. - Source: PubMed
Publication date: 2026/04/13
Magnolia Martínez-AguilarZeinab AbdullahHans BlokzijlHan Moshage - Pancreatic cancer (PC) is a common gastrointestinal malignancy whose initiation and progression may be closely linked to the gut microbiota. Previous research indicates that Scutellaria barbata D. Don and Scleromitrion diffusum (Willd.) R.J. Wang (SB-SD) exhibit diverse biological activities, such as anti-inflammatory, antioxidant, and antitumor effects, though their precise regulatory mechanisms are not fully elucidated. Here, we treated PC cells with SB-SD to assess its impact on cell viability, apoptosis, migration, and cell cycle progression, while Western blotting analyzed the expression of HSP90AA1, MAPK3, p53, CDK1, and p21. We also established a pancreatic cancer xenograft model in nude mice to evaluate the in vivo inhibitory effect of SB-SD on tumor growth. Furthermore, we employed metagenomic sequencing, untargeted metabolomics, and quantitative proteomics to comprehensively profile changes in the gut microbiota, serum metabolites, and differentially expressed proteins, with Western blotting subsequently validating BCKDK, GATM and p53 expression. The results show that SB-SD significantly inhibited PC cell proliferation, promoted apoptosis, and induced S/G2 phase cell cycle arrest, potentially via modulation of the HSP90AA1/MAPK3 signaling pathway. Measurements of tumor volume and weight, complemented by histopathological analysis, confirmed that SB-SD effectively suppressed the growth of PANC-1 xenograft tumors. Integrated multi-omics analyses suggest that the antitumor effects of SB-SD may involve the modulation of key gut microbes like Bacteroides caccae and Lactobacillus, the promotion of choline metabolism, and the regulation of BCKDK and GATM. Together, these findings not only corroborate the direct antitumor activity of SB-SD against pancreatic cancer but also offer novel mechanistic insights by constructing a microbiota-metabolite-protein interaction network. - Source: PubMed
Publication date: 2026/03/27
Zhao ZhihaoYang YutongZhang LiuHe XuDing KaiyueChen YingtingHuo YuexueLi PeiyuLi RuotongAli TanveerZhao DanpingChoe HyokcholMa JunnanShang DongZhang Lin - Nutrient competition between tumor and immune cells is a hallmark of the glioblastoma (GBM) microenvironment, yet the mechanisms underlying amino acid metabolic reprogramming and immune evasion remain incompletely understood. Here, we demonstrate that GBM cells outcompete NK cells for branched-chain amino acid (BCAA), leading to BCAA depletion, suppression of NK and CD8 T cell cytotoxicity, and immune escape. Mechanistically, we identify a positive feedback circuit involving PSMD14, BCKDK, and IGF2BP3 that stabilizes BCKDK post-translationally and promotes SLC7A5/SLC7A8-mediated BCAA uptake by GBM cells. PSMD14 directly interacts with and deubiquitinates BCKDK, antagonizing TRIM21-mediated proteasomal degradation. This metabolic remodeling disrupts NK cell signaling and function, as BCAA deprivation impairs PI3K/Akt and cGAS-STING pathways and disrupts mitochondrial integrity. Preclinical models reveal that pharmacologic inhibition of PSMD14 by O-phenanthroline (OPA) or PSMD14 knockdown restores immune cell infiltration, enhances CAR-NK cytotoxicity, and synergizes with immunotherapy to suppress GBM growth. Clinical analysis further establishes that elevated PSMD14 and BCKDK expression in GBM correlates with decreased CD8 T and NK cell infiltration and poorer patient survival. These findings highlight the PSMD14-BCKDK axis as a central regulator of tumor metabolic adaptation and immune suppression, and support PSMD14 inhibition-alone or in combination with CAR-NK therapy-as a promising strategy for precision immunometabolic intervention in GBM. - Source: PubMed
Publication date: 2026/03/25
Yu ShaojieWang MinjieJiang ChengLi XudongWang XuanCheng QihongGong ZihanZhao ZhenHe JieXiang WeiLi JunjunJiang Xiaobing - Metabolic reprogramming of Branched-chain amino acids (BCAAs)-leucine, isoleucine, and valine-has emerged as a constitutive feature of cancer, extending far beyond their canonical roles in protein synthesis and energy provision. In malignancy, these essential amino acids function as pivotal signaling mediators and epigenetic modulators, thereby propelling tumor progression, facilitating immune evasion, and conferring resistance to therapeutic agents. This review delineates how cancer cells subvert branched-chain amino acid metabolism to fuel anabolic processes, activate oncogenic signaling cascades including mTOR and PI3K/AKT, and remodel the tumor microenvironment. A framework is presented to categorize the differential reliance of various cancers on key catabolic enzymes-BCAT1, BCAT2 and BCKDK-underscoring their therapeutic vulnerability. The paradoxical role of BCAAs in modulating anti-tumor immunity is examined alongside the potential of dietary modulation and the development of pharmacological inhibitors targeting this pathway. Concluding perspectives highlight the trajectory for translating these insights into precision oncology, advocating for biomarker-guided and context-specific therapeutic strategies. - Source: PubMed
Publication date: 2026/02/13
He BinfanLi LingxiLiu YeHao MengmengZhang LingHe Rongzhang