Mouse DLAT (Dihydrolipoyl Transacetylase) ELISA Kit
- Known as:
- Mouse DLAT (Dihydrolipoyl Transacetylase) Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- E-EL-M0416
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- Elabscience
- Gene target:
- Mouse DLAT (Dihydrolipoyl Transacetylase) ELISA Kit
Related genes to: Mouse 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
Related products to: Mouse DLAT (Dihydrolipoyl Transacetylase) ELISA Kit
Related articles to: Mouse DLAT (Dihydrolipoyl Transacetylase) ELISA Kit
- Autoantibodies against tumor-associated antigens in plasma are valuable biomarkers for early cancer detection and prognostic stratification. Dihydrolipoamide acetyltransferase (DLAT) and lipoic acid synthetase (LIAS), two key cuproptosis regulators, are abnormally expressed in non-small cell lung cancer (NSCLC) and are potential biomarkers for clinical diagnosis. This study explored the significance of anti-DLAT and anti-LIAS autoantibodies in the clinical diagnosis and prognosis of NSCLC. - Source: PubMed
Publication date: 2026/05/27
Liu AichenZhang LuluYu PeiqiNie TingzunCao XiaobinLi JingSun WenkeLiang YihaoOuyang SongyunDai LipingLiu Jingjing - Rheumatoid arthritis (RA) is characterized by severe synovial inflammation and progressive joint destruction. This study evaluated the therapeutic effects of electroacupuncture (EA) in a rat model of RA and explored its potential association with lipoic acid (LA) metabolism. Collagen-induced arthritis (CIA) was established in rats, followed by EA stimulation at ST36 (Zusanli) for 14 d. Hind-paw thickness and arthritis index scores were assessed weekly. On day 28, synovial histopathology was examined by hematoxylin and eosin staining. Serum cytokine levels were measured by ELISA. Synovial tissue metabolomics was performed to identify EA-responsive metabolic pathways, and candidate proteins were validated by Western blotting. Serum copper (Cu2+) levels were also quantified. The results demonstrated that EA alleviated CIA manifestations in an intensity-dependent manner, with low-intensity stimulation (0.5 mA) showing the greatest efficacy. EA reduced joint damage and systemic inflammation, as reflected by increased IL-10 and decreased TNF-α, IL-6, and IL-17 levels. Metabolomic analysis highlighted alterations in LA metabolism. Protein levels of DLAT and LIAS were elevated in CIA rats and were reduced after EA or methotrexate treatment. Serum Cu2+ levels exhibited a similar trend. In conclusion, low-intensity EA attenuates joint inflammation in CIA rats, potentially through modulation of LA metabolism and associated copper homeostasis, providing new metabolic insights into its anti-inflammatory effects in RA. - Source: PubMed
Shen ChuchuQiu ShuoJiang Xin-XueLian Jian-FengXia Xue-FengXu Sen-LeiLin YingZhang Hong-Ru - Mild cognitive impairment (MCI), a condition that falls somewhere between normal aging and severe cognitive dysfunction (e.g., Alzheimer's disease), is a common manifestation of the neurocognitive function decline that seniors encounter as they age. The fundamental processes causing its beginning are still not well understood yet. - Source: PubMed
Publication date: 2026/05/13
Wang BoZhang JingLi Chang-HongHuang XiaoGao Ruo-BingPeng YanXie QingNing Ya-LeiZhao YanYang NanChen XingXie Yang-LiZhou Yuan-GuoLin SenChen LinLi Ping - : 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