DLAT siRNA_Lentivectors
- Known as:
- DLAT siRNA_Lentivectors
- Catalog number:
- i006170d
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- DLAT siRNA_Lentivectors
Related genes to: DLAT siRNA_Lentivectors
- 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
Related products to: DLAT siRNA_Lentivectors
Related articles to: DLAT siRNA_Lentivectors
- : This study investigates the induction of cuproptosis in A549 lung cancer cells by doxorubicin (DOX) complexes and the development of pH-responsive bovine serum albumin (BSA)-based nanocarriers for their delivery. We successfully synthesized and characterized two novel complexes: DOX-Cu, where DOX acts as a ligand for Cu(II), and DOX-BTZ, a conjugate formed between DOX and the proteasome inhibitor bortezomib (BTZ). : Spectroscopic and NMR analyses were performed to confirm the formation of the complexes. In vitro assays were conducted to evaluate cytotoxicity in A549 cells, alongside assessment of DLAT aggregation as a marker of cuproptosis. The formulation of DOX into BSA nanoparticles (DOX-Cu@BSA NPs and DOX-BTZ@BSA NPs) was carried out to evaluate potential alleviation of DOX-induced cytotoxicity in cardiomyocytes in vitro. Fluorescence quenching and molecular docking studies were employed to investigate the binding interactions between the complexes and BSA. Cellular uptake experiments were performed to assess nanoparticle internalization into A549 cells. : Both complexes exhibited superior cytotoxicity against A549 cells compared to individual components. This enhanced cell death was associated with significant aggregation of dihydrolipoamide S-acetyltransferase (DLAT), a key marker of cuproptosis, suggesting the involvement of this copper-dependent cell death pathway. The BSA nanoparticles displayed favorable characteristics, including uniform size (~190 nm), high encapsulation efficiency (~75-79%), and colloidal stability. Crucially, they exhibited a pH-responsive drug release profile, with significantly accelerated release under acidic conditions (pH 5.7) mimicking the tumor microenvironment. Fluorescence quenching and molecular docking studies revealed strong, spontaneous binding between the complexes and BSA, primarily driven by hydrophobic interactions. Cellular uptake experiments confirmed efficient internalization of the nanoparticles into A549 cells. : Collectively, this work offers a proof-of-concept for a strategy of utilizing BSA-based multidrug delivery systems for cuproptosis induction, offering a potential avenue to enhance therapeutic efficacy while reducing systemic toxicity in lung cancer treatment. - Source: PubMed
Publication date: 2026/04/26
Zhang HaiyingChen XuanjiaQiao ShihuiMeng HuanfengLong HuiZhong HuaminLiu YihengSong YunGao YananLiu YanMao Lujia - The pathogenic mechanisms of osteoporosis (OP), a systemic metabolic bone disease marked by an imbalance between bone growth and resorption, are still not fully understood.Through the specific binding of copper ions to mitochondrial the tricarboxylic acid (TCA) cycle acyl-CoA deoxygenases (like DLAT and PDHA1), cuproptosis-a novel copper-dependent form of programmed cell death-causes protein toxicity stress, protein aggregation, and iron-sulfur cluster (Fe-S cluster) depletion. This finding provides a fresh viewpoint on how to explain the molecular processes underlying oxidative stress.This study offers a comprehensive analysis of the fundamental molecular processes behind cuproptosis, with an emphasis on how it is regulated specifically in bone metabolism. These mechanisms include the regulation of copper homeostasis, FDX1-mediated lipoylation modification, and Fe-S cluster metabolic disturbance. We hypothesize that the RUNX2-PDHA1 axis may underlie the high mitochondrial respiration dependence and enhanced lipoylase expression that could render osteoblasts sensitive to cuproptosis, while osteoclasts are naturally resistant due to their reliance on glycolysis and the RANKL-ERK1/2 pathway-mediated inhibition of lipoylation.Furthermore, genes linked to cuproptosis (PDHA1, FDX1, and CDKN2A) control metabolic reprogramming, the linkage between oxidative stress and inflammation, and cellular senescence, all of which contribute to the development of OP. An additional factor contributing to bone metabolic imbalance is the cuproptosis-dependent control of T-cell cytokine production and macrophage polarization in the bone immunological milieu. According to a theoretical framework for creating focused therapeutic techniques, copper-induced death contributes to OP disease through a cascade process that includes "copper metabolism abnormalities - cell-specific differential death - immune microenvironment disruption." - Source: PubMed
Publication date: 2026/05/21
He JunboLi FeilongYuan HaoxiangLiu JianiPeng YongWu HaozheLuo YingjinLi FengjiangXu WenboSong ChaoHao PandengLiu Zongchao - Copper oxide nanoparticles (CuO NPs) are widely used in agriculture, medicine, food, and electronic materials, raising increasing concerns about their potential health risks. Nanoparticles (NPs) can cross biological barriers and enter the bloodstream, making the cardiovascular system a potential target of toxicity. However, the endothelial toxicity of CuO NPs and the size dependent mechanisms underlying their effects remain unclear. In this study, the cytotoxicity of CuO NPs with different sizes in human umbilical vein endothelial cells (HUVECs) and the underlying mechanisms were investigated. CuO NPs reduced cell viability, increased LDH release, and inhibited cell proliferation in a size dependent manner (5 nm > 20 nm > 80 nm). Smaller CuO NPs induced higher ROS levels, disrupted the antioxidant system, and caused mitochondrial dysfunction, ultimately resulting in cuproptosis in HUVECs, as evidenced by DLAT aggregation and Fe-S proteins loss. In addition, CuO NPs activated the MAPK, NF-κB NLRP3 inflammasome and DNA damage response (DDR) pathway. Overall, CuO NPs induced size-dependent endothelial injury through oxidative stress, inflammation, DNA damage, and cuproptosis by activating MAPK/NF-κB/NLRP3 and the DDR pathway. These findings provide mechanistic insights into the cardiovascular toxicity of CuO NPs and support risk assessment of nanomaterial exposure. - Source: PubMed
Publication date: 2026/05/21
Cheng YeCao XiangyuLiu Dawo - Sepsis-induced myocardial injury (SIMI) has become an important cause of death in septic patients, and it is a multi-faceted pathophysiological process. The present study aims to understand how insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) regulates cardiomyocyte cuproptosis through an mA-dependent regulation of mitogen-activated protein kinase kinase 1 (MAP2K1), and advance our knowledge of SIMI. - Source: PubMed
Publication date: 2026/05/10
Chen RuiyaoLu LuLin BeibeiChen ChengjieLiang Yafeng - Hepatocellular carcinoma recurrence after microwave ablation commonly results from residual micrometastases and an immunosuppressive tumor microenvironment. To address these dual barriers, this study developed a combined strategy using ultrasound-guided microwave ablation alongside lipopolysaccharide. Through multimodal experimental approaches, the combination therapy induced interconnected therapeutic cascades: immunogenic remodeling via M1 macrophage polarization with anti-angiogenic effects; features of ferroptosis, including NRF2 suppression, glutathione depletion, and cytoplasmic lipid peroxidation; and Hsp70-mediated proteostasis counteracting copper toxicity despite modulation of the FDX1-LIAS-DLAT axis. Adaptive stress responses limited copper-dependent cell death, while prominent cytoplasmic lipid peroxide accumulation was observed spatially. This work establishes a distinctive paradigm combining localized thermal stress and macrophage reprogramming to effectively suppress post-ablation recurrence, transforming microwave ablation into a platform for systemic immunotherapy in hepatocellular carcinoma management. - Source: PubMed
Publication date: 2026/04/01
Sui YajuanPeng JiahuiMeng WenyiLi RenjieKang YangLi LujingXu Zuofeng