DLAT Antibody (C_term)
- Known as:
- DLAT Antibody (C_term)
- Catalog number:
- AP5341b
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- DLAT Antibody (C_term)
Related genes to: DLAT Antibody (C_term)
- 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 Antibody (C_term)
Related articles to: DLAT Antibody (C_term)
- 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 - Recent pharmacological breakthroughs have identified cuproptosis as a distinct, regulated cell death (RCD) pathway driven by mitochondrial copper overload. Unlike traditional RCDs such as apoptosis or ferroptosis, cuproptosis is characterized by the direct binding of excess copper to lipoylated enzymes of the tricarboxylic acid (TCA) cycle, notably the E2 subunit of pyruvate dehydrogenase (DLAT). This interaction triggers toxic protein aggregation and the destabilization of iron-sulfur (Fe-S) cluster proteins, culminating in metabolic collapse. This review provides an updated and integrative overview of the molecular machinery governing copper homeostasis, highlighting ferredoxin 1 (FDX1) and lipoyl synthase (LIAS) as pivotal metabolic gatekeepers. We summarize opportunities and unresolved challenges in leveraging copper ionophores (e.g., elesclomol and disulfiram) and high-affinity chelators (e.g., tetrathiomolybdate) across malignant and non-neoplastic diseases. Furthermore, we address the translational challenges of precision delivery, including the use of nanoparticle-based systems to enhance therapeutic indices and the identification of biomarkers for patient stratification. By integrating recent pre-clinical and early clinical data (2023-2025), we suggest that targeting the mitochondrial-copper axis represents a promising, yet still experimentally grounded, avenue in precision medicine, while emphasizing current limitations in biomarker validation, delivery selectivity, and safety profiling. - Source: PubMed
Publication date: 2026/04/18
El-Nablaway MohammadAttia Mohamed IbrahimYousef Tarek AKoushaji GhaithTarik WedadGilkaramenthi RafiullaElazab Khalid M - The prognostic values of cuproptosis-related genes (CRGs) in gastric cancer with lymph node metastasis (GCLM), especially in the tumor immune microenvironment (TIME), remain unclear. We analyzed the expression, mutation, immunity, drug sensitivity, and prognostic value of CRGs in GCLM using TCGA and GEO cohorts. Consensus clustering was performed to identify CRG subtypes, with differences characterized by multi-omics analysis. A CRG-based prognostic risk score and immune score were constructed for individualized assessment, and the role of CRGs was validated through in vitro and in vivo experiments. Consensus clustering revealed that CRGs were significantly enriched in biological processes related to mitosis and energy metabolism, as well as in immune-related and cancer-associated pathways. Four distinct CRG subtypes were identified, showing marked differences in expression profiles, prognosis, genetic alterations, TIME, and chemotherapeutic drug sensitivity. We developed an exploratory CRG-based prognostic risk score for preliminary individualized assessment, and the functional relevance of CRGs in GCLM was further validated through in vitro experiments. Among these, FDX1, LIAS, DLAT, MTF1, and GLS were identified as key determinants of overall survival in patients with GCLM, with FDX1 emerging as a potential independent prognostic factor. Notably, upregulation of FDX1 significantly suppressed lymph node metastasis of gastric cancer cells in a mouse popliteal lymph node metastasis model. Our data uncovers FDX1 might be a potential favorable prognostic factors in GCLM patients. These findings may improve our understanding of CRGs in GCLM and provide new in-sights for assessing prognosis and developing more effective treatment strategies. - Source: PubMed
Publication date: 2026/05/10
Zhang TianhaoLiu JianqiuDuan PengLi ZikangHuang ZhixinZhao ZeyuCheng YangLiang ZhiChen JianhuiCai MeilanMa Jinping - Cuproptosis, an emerging form of programmed cell death, is capable of inducing mitochondrial dysfunction. Moreover, the PI3K-AKT-mTOR signaling pathway contributes to tumor cell progression by reprogramming mitochondrial morphology and function. In this study, we have designed copper complex nanoparticles (NP) and PI3K-AKT-mTOR inhibitor Alpelisib nanoparticles (NP) that enhance the efficacy of cuproptosis-based therapies. NP triggers mitochondrial dysfunction and promotes the aggregation of lipoylated dihydrolipoamide S-acetyltransferase (DLAT), while NP inhibits the PI3K-AKT-mTOR signaling pathway to induce apoptosis. The combination of these two nanoparticles (NP+NP) effectively activates the antitumor responses in the tumor microenvironment (TME). When combined with an anti-programmed cell death protein 1 antibody (α-PD-1), NP+NP significantly inhibits tumor progression and activates antitumor immunity, offering a promising strategy for liver cancer treatment. - Source: PubMed
Publication date: 2026/05/05
Wu LeiNa JintongLiu XiyuTang DongshengYang ZhungangCao ZhengHe XinyueXiao HaihuaZhong LipingLiao YuanZhao Yongxiang - Cuproptosis represents a promising therapeutic strategy for cancer; however, its clinical application remains limited. We observed elevated copper levels and increased expression of DLAT, a key procuproptosis gene, in colorectal cancer (CRC) tissues, suggesting inherent susceptibility to cuproptosis. Furthermore, NAT10 enhances DLAT mRNA stability by mediating its N-acetylcytidine (ac4C) modification, thereby promoting cuproptosis. We also discovered that lactylation of NAT10 at lysine 426 (K426) enhances NAT10 catalytic activity. Conversely, SIRT1 mediates the delactylation of NAT10-K426, leading to the inhibition of cuproptosis. The combination of elesclomol (a cuproptosis inducer) and selisistat (a SIRT1 inhibitor) effectively induced cuproptosis in CRC. Notably, the reduction of soluble DLAT induced by elesclomol treatment was found to enhance NAT10-K426 lactylation. Moreover, DLAT supplementation establishes a positive feedback loop that amplifies cuproptosis. These results underscore the critical role of nonhistone NAT10 lactylation in tumor cuproptosis and highlight the therapeutic potential of targeting this pathway for CRC treatment. - Source: PubMed
Publication date: 2026/05/05
Yang Wen-DongLu Meng-RuShen QiZhou Pei-HengDiao YangXia ShanLu Ya-ChunCui Yong-QiangLi Bing-QiangXu Wen-XiaChen LinZhang ChaoMa NingGuo YaoShao Zhi-YingGe Wen-JieBai Jin