Porcine DLAT (Dihydrolipoyl Transacetylase) ELISA Kit
- Known as:
- Porcine DLAT (Dihydrolipoyl Transacetylase) Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- e-el-p0725
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Elabscience
- Gene target:
- Porcine DLAT (Dihydrolipoyl Transacetylase) ELISA Kit
Related genes to: Porcine DLAT (Dihydrolipoyl Transacetylase) ELISA Kit
- Gene:
- DLAT NIH gene
- Name:
- dihydrolipoamide S-acetyltransferase
- Previous symbol:
- DLTA
- Synonyms:
- PDC-E2, E2
- Chromosome:
- 11q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2018-12-14
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- Acute liver injury, a critical complication of severe malaria, was characterized by hepatocyte death and hepatic stellate cell (HSC) activation. While HSC activation was a well-established driver of chronic liver fibrosis, its specific role and the triggers initiating it during the acute phase of malarial liver injury remain poorly defined. Notably, systemic copper accumulation occurred during Plasmodium infection and can induce cuproptosis, a novel form of copper-dependent mitochondrial cell death. Given the liver's central role in copper metabolism and storage, coupled with the known sensitivity of HSC to copper perturbations, we hypothesized that malaria-induced hepatic copper overload may trigger cuproptosis, which subsequently acted as a key signal promoting HSC activation, thereby exacerbating acute liver injury. - Source: PubMed
Publication date: 2026/06/08
Mo XiumeiChen QianZhong RuiLin YannanLiu ZhiqiZhang XiaoranHou XinpengLin HaofengZhang MinLiu WenbinHe JiajingChen ZhiyuYe MinqiuDeng ZujunJin XiaobaoLiu ZhenlongSong JianpingYin HuiHuang Bo - Increasing studies have found links between immune traits and intrahepatic cholangiocarcinoma (ICC). However, the presence of confounding variables makes it difficult to determine if this correlation shows a real cause-and-effect relationship. - Source: PubMed
Publication date: 2026/05/22
Ye ZhipengTang BuLangZhang YuanjianChen HanhanLi JieYe ZhitaoLiu XuejianLi Di - Cuproptosis, has attracted increasing attention in cancer therapy due to its apoptosis-independent mechanism and potential to overcome drug resistance. However, current copper-mediated nanotherapeutics are still limited by low drug-loading efficiency and insufficient therapeutic versatility. Herein, a tumor microenvironment-responsive nanoplatform, HA-SiO@ESCu-Hemin (SNECHA), was developed for combined cuproptosis-photothermal therapy. Dendritic SiO nanoparticles were sequentially loaded with elesclomol-copper complex (ESCu) and hemin, followed by hyaluronic acid (HA) coating to achieve CD44-mediated tumor targeting and HAase/pH-responsive drug release. After internalization, ESCu induced cuproptosis through FDX1-mediated copper reduction, Fe-S cluster disruption, and DLAT-associated proteotoxic stress, while hemin enabled 808 nm laser-triggered photothermal therapy. SNECHA showed efficient near-infrared photothermal conversion with an efficiency of 46.69% and increased to 57.3 °C. In addition, it exhibited enhanced cellular uptake, selective cytotoxicity toward A549 cells with IC value of 103.2 nM under laser illumination, and significantly improved antitumor efficacy. In vivo results further demonstrated enhanced tumor accumulation, superior tumor growth inhibition, and favorable preliminary biosafety. This work provides a targeted nanotherapeutic strategy for enhanced cancer treatment through cuproptosis-photothermal combination therapy. - Source: PubMed
Publication date: 2026/06/02
Li XiaojieLi ChunlinLiu DiWang Yonglian - Hepatocellular carcinoma (HCC) is the primary type of liver malignancy, which stands as the third leading contributor to cancer-related death worldwide. Sodium butyrate (NaB), a gut microbiota-derived short-chain fatty acid with known anticancer activity, remains poorly understood in HCC. This study aimed to elucidate the effects and underlying mechanisms of NaB-induced cuproptosis in HCC cells. 200 mg/kg NaB inhibits HCC tumor growth by 73.9% and induced a 1.83- and 6.83-fold increase in the Cu content and SLC31A1 protein expression, respectively. Furthermore, 5 mmol/L NaB inhibits cell viability by 35.4% and induced a 1.52-, 2.20-, 7.96-, 2.34-, and 2.24-fold increase in the cell number in G1 phase, Cu content and protein expression of SLC31A1, FDX1 and lipoic DLAT, respectively. NaB inhibits viability and cell cycle progression and promotes cuproptosis in HCC cells, which were revised by SLC31A1. NaB induces SLC31A1 expression by inhibiting HDAC1-induced decrease in the levels of H3K27ac, thus inhibiting HepG2 cell growth and promoting cuproptosis. SLC31A1 mRNA is positively correlated with Cu concentration, while HDAC1 mRNA is negatively correlated with both Cu concentration and SLC31A1 mRNA in patients with HCC. In conclusion, our findings indicate that NaB inhibits the HCC cell growth by targeting HDAC1-SLC31A1 axis-dependent cuproptosis. - Source: PubMed
Publication date: 2026/06/02
Zeng HuiZhang ZheweiJiang YurouChen PengtaoChu Xiaofeng - Metastatic progression is the leading cause of mortality in lung adenocarcinoma (LUAD), yet how oncogenic signals are translated into stable metabolic and epigenetic programs that sustain tumour progression remains poorly understood. Here, through integrated single-cell, bulk, and spatial transcriptomic analyses, we identify the orphan G protein-coupled receptor GPR87 as a progression-associated regulator linked to enhanced glycolytic activity and adverse clinical outcome in LUAD. Mechanistically, GPR87 activates the cAMP/PKA/CREB pathway to induce acetyl-CoA synthetase 2 (ACSS2) transcription, thereby promoting histone H3 lysine 27 lactylation (H3K27la). H3K27la directly enhances transcription of dihydrolipoamide S-acetyltransferase (DLAT), reinforcing glycolytic flux and lactate production in a self-sustaining metabolic-epigenetic circuit. In parallel, GPR87 physically stabilizes lactate dehydrogenase A (LDHA), further amplifying lactate output. Genetic disruption of ACSS2 suppresses GPR87-driven tumour growth and metastatic colonization in vivo. Consistently, coordinated activation of this axis is enriched in advanced-stage human LUAD. Together, these findings define a GPR87-centred metabolic-epigenetic circuit that sustains glycolytic dominance and supports LUAD progression and metastasis. - Source: PubMed
Publication date: 2026/06/01
Zhang YuLi XinHan RongGuo MingyuanLin EnguangYang ChenNing JinfengZhao Yanbin