DLAT
- Known as:
- DLAT
- Catalog number:
- ARP41995_P050
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- DLAT
Related genes to: DLAT
- 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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- 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. 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 - Humans change their exposure to risks either actively, by taking deliberate actions, or passively, through inaction. These different modes of choice may result in varying levels of risk exposure. This study introduces a novel experimental task, the Dynamic Lottery Adjustment Task (DLAT), to investigate the effects of active versus passive risk-taking across two related experiments. The DLAT addresses a gap in the literature, as existing incentivized risk measures exclusively target active risk-taking. Consequently, differences between active and passive risk-taking have previously been studied only through non-incentivized surveys and vignettes focusing on specific choice domains (e.g., vaccination decisions). The first study, a controlled laboratory experiment, shows little variation in risk-taking between active and passive choice modes, contradicting existing findings of a general "passive-is-less-risky" bias. Conversely, the second experiment, conducted online over ten days, introduces higher attention costs and provides strong evidence that these costs significantly influence risk-taking behaviors in more naturalistic decision-making environments. Our findings highlight the importance of considering situational factors, such as attention costs, in understanding how different choice modes affect risk-taking in real-life settings, including financial investments, health behaviors, or career choices. - Source: PubMed
Publication date: 2026/05/13
König-Kersting ChristianLohse JohannesMerkel Anna Louisa