Porcine Dihydrolipoyl Transacetylase ELISA , DLAT
- Known as:
- Porcine Dihydrolipoyl Transacetylase Enzyme-linked immunosorbent assay test , DLAT
- Catalog number:
- E07D0021
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Porcine Dihydrolipoyl Transacetylase ELISA DLAT
Related genes to: Porcine Dihydrolipoyl Transacetylase ELISA , 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
Related products to: Porcine Dihydrolipoyl Transacetylase ELISA , DLAT
Related articles to: Porcine Dihydrolipoyl Transacetylase ELISA , DLAT
- Metabolic cell death (MCD) modulates colorectal cancer (CRC) progression, yet its prognostic value remains unexplored. We aimed to build an MCD-centred gene signature for outcome prediction and precision therapy. - Source: PubMed
Publication date: 2026/07/16
Zhuang WeiZhang YaLiu ZhengyongYan WenxueWei TaoDeng QiupingLiu Qi - Intrauterine adhesion (IUA) significantly contributes to female infertility, primarily characterized by abnormal fibrotic remodeling of the endometrium. The intricate interplay among various cellular components within the endometrial microenvironment plays a pivotal role in IUA pathophysiology. Among these implicated factors, the vitamin D receptor (VDR) has emerged as a potential regulator of fibrotic processes; however, its specific role and underlying mechanisms in IUA remain inadequately understood. This study aimed to investigate the role of VDR in IUA pathogenesis and its impact on endometrial macrophage behavior. - Source: PubMed
Publication date: 2026/09/05
Yong MinWu XixiHu Jianguo - Multidrug-resistance (MDR) remains a formidable obstacle in the treatment of breast cancer, primarily due to the overexpression of P-glycoprotein (P-gp) efflux pumps. The objective of this study is to develop a copper-based nanotherapeutic agent capable of simultaneously inhibiting drug efflux and inducing a novel form of cell death, cuproptosis, to overcome MDR. The nanoparticle known as DOX-P-gp ASO-Cu NPs has been engineered to facilitate the delivery of doxorubicin (Dox), P-gp antisense oligonucleotide (P-gp ASO), and copper ions into cancer cells. The incorporation of ASO effectively silenced P-gp expression, significantly enhancing the retention of Dox within the cells. Consequently, the IC value of Dox in the nanoparticle formulation was reduced by 17.5-fold compared to free Dox in MCF-7/ADM cells. This synergistic strategy not only restored chemosensitivity but also triggered cuproptosis, as evidenced by mitochondrial dysfunction, downregulation of LIAS/FDX1, and DLAT oligomerization. The results of drug-resistant breast cancer xenograft model further demonstrated superior tumor suppression with the nanoformulation compared to monotherapy. This integrated strategy, which involves the inhibition of drug efflux and the induction of cuproptosis, offers a promising approach to eradicating multidrug-resistant breast cancer. - Source: PubMed
Publication date: 2026/08/31
Kou ShixuZhang YuChe XinyuDuan WangdaYang ZhaoqiWang Teng - Copper is an essential trace element required for mitochondrial respiration, redox regulation, iron metabolism, and cellular signalling, but excessive or mislocalised copper can be cytotoxic. Cuproptosis is a recently identified form of regulated cell death in which copper binds to lipoylated mitochondrial proteins, promotes their aggregation, destabilises iron-sulfur cluster proteins, and induces mitochondrial proteotoxic stress. Copper therefore has context-dependent roles in cancer. Physiological copper supports tumour metabolism, angiogenesis, extracellular-matrix remodelling, and selected oncogenic signalling pathways, whereas therapeutic copper depletion can inhibit copper-dependent tumour processes. Conversely, copper ionophores and related approaches may increase intracellular copper sufficiently to induce cuproptosis in metabolically susceptible cancer cells. This review describes systemic and intracellular copper homeostasis, including intestinal absorption, intracellular trafficking, mitochondrial copper distribution, storage, and export. Particular attention is given to CTR1/SLC31A1, the functionally distinct copper-transporting ATPases ATP7A and ATP7B, metallothioneins, copper chaperones, and cytochrome c oxidase assembly factors. We also examine how cancer cells reprogramme copper handling to support proliferation, angiogenesis, metastasis, and immune evasion. Finally, we discuss the molecular basis of cuproptosis, including the roles of FDX1, FDXR, LIAS, DLAT, mitochondrial respiration, protein lipoylation, and iron-sulfur cluster destabilisation. Current evidence indicates that cuproptosis susceptibility varies among tumour types and depends on copper handling, mitochondrial metabolic state, and the integrity of the protein-lipoylation machinery. Defining these determinants will be necessary for the development of tumour-selective copper-targeted therapies. - Source: PubMed
Publication date: 2026/09/03
Eshraghi RezaHosseini NastaranYazdani Mohammad SepehrBadihi ShirinPirmoradian PedramBahrami AshkanDarouei BaharGhanouni ShayanLam Alfred KHamblin Michael R - Rapidly progressive pneumoconiosis (RPP) is an aggressive subtype of pneumoconiosis characterized by persistent pulmonary inflammation, rapidly progressive fibrosis, and early-onset progressive massive fibrosis. However, the systemic molecular alterations of RPP remain unclear. Here, we profiled the plasma proteome to identify candidate proteins associated with RPP, aiming to discover potential peripheral biomarkers for this aggressive phenotype. - Source: PubMed
Publication date: 2026/08/14
Tang MeianLuo YufeiLi YingTang WeiweiYi XiaZhang XiaohuaWang LimingChen Rou