DLAT Antibody
- Known as:
- DLAT Antibody
- Catalog number:
- XW-8135
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- DLAT Antibody
Related genes to: DLAT Antibody
- 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
Related articles to: DLAT Antibody
- 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 - Cuproptosis, a recently identified form of programmed cell death, has an unclear role in the context of metabolic dysfunction-associated steatohepatitis (MASH). This study aims to elucidate the role of cuproptosis in the early stages of MASH progression, identify its primary regulatory factors, and delineate the associated molecular mechanisms. - Source: PubMed
Publication date: 2026/05/02
Fu XuanLi YunmengChen JingYin BaolongNasrin MahbubaHuo RuiTian Shuxin - Bortezomib (BTZ), the first-generation proteasome inhibitor, has been approved for the treatment of relapsed, refractory, and newly diagnosed multiple myeloma. Despite its remarkable antitumor efficacy, BTZ treatment is severely limited by a high incidence of systemic adverse reactions, primarily due to its non-selective cytotoxicity toward rapidly dividing normal cells and its potent neurotoxic effects on peripheral neurons. Bortezomib-induced peripheral neurotoxicity (BIPN) manifests as neuropathic pain and sensory abnormalities, affecting up to 31% to 64% of patients and limiting BTZ's clinical use. Currently, the underlying mechanisms of BIPN are poorly understood. To evaluate the effects of BTZ on the functions of peripheral nerves in mice, we administered an intraperitoneal injection treatment for four weeks. Results indicated that BIPN caused mechanical allodynia, gait abnormalities, and pathological changes in myelin and axons in mice. This study confirms that BTZ upregulates the expression of the activating transcription factor 3 (ATF3), which in turn mediates the increased expression of the copper transporter SLC31A1, causing dysregulation of intracellular copper ion homeostasis and subsequent copper accumulation, and ultimately inducing the development of peripheral neurotoxicity. Elevated intracellular copper concentration exerts a dual effect: it directly promotes the oligomerization of Dihydrolipoamide S-acetyltransferase (DLAT) and concurrently damages the iron-sulfur cluster protein ferredoxin 1 (FDX1), collectively triggering the onset of cuproptosis. Green tea has garnered attention for its rich content of catechins, with (-)-Epigallocatechin Gallate (EGCG) being the most abundant catechin present. This study uncovers the molecular mechanism by which EGCG inhibits BTZ-induced cuproptosis through targeted regulation of copper homeostasis. Analyses demonstrate that EGCG significantly downregulates the expression of the copper transporter SLC31A1, thereby effectively suppressing transmembrane influx of extracellular copper ions. This intervention markedly reduces intracellular copper overload, eliciting a dual regulatory effect: on one hand, the decreased copper concentration directly inhibits the oligomerization of DLAT; on the other hand, it effectively protects the iron-sulfur cluster protein FDX1 from damage. This study aims to systematically elucidate the molecular mechanisms underlying BIPN and to evaluate the therapeutic potential of EGCG in alleviating BIPN, offering a novel therapeutic strategy for the prevention and treatment of BIPN. - Source: PubMed
Publication date: 2026/04/21
Wang YonghaiLu JiabinFeng XuejingYang BoHe QiaojunLuo PeihuaYang Xiaochun - Resveratrol (Res), a natural polyphenolic compound, exhibits multiple antitumor activities against acute myeloid leukemia (AML), though its mechanisms remain incompletely understood. In this study, CCK-8 assay, CFSE flow cytometry, Transwell assays, and flow cytometry assessed proliferation, invasion, migration, and programmed cell death in MV4-11 and MOLM-13 leukemic cell lines. Western blotting examined cell death regulatory factors (Cleaved-caspase 3/caspase 3, Bax, Bcl-2), aerobic glycolysis proteins (GLUT1, HK2, LDHA, PKM2), cuproptosis-related proteins (FDX1, DLAT, Lip-DLAT, DLST, Lip-DLST, HSP70, SDHB), and PI3K/AKT pathway proteins (p-PI3K/PI3K, p-AKT/AKT). Intracellular Cu⁺ levels were measured colorimetrically, while glucose uptake, lactate, and ATP levels were quantified to evaluate cellular metabolism. Mechanistic investigations utilized PFKFB3 overexpression, PI3K activator (740 Y-P), and inhibitor (LY294002) intervention experiments. The antitumor efficacy of Res was validated in an AML xenograft mouse model. Res significantly inhibited AML cell proliferation, invasion, and migration while promoting apoptosis. It markedly downregulated FDX1, Lip-DLAT, Lip-DLST, and SDHB while upregulating HSP70 and intracellular Cu⁺, inducing cuproptosis-an effect reversible by the cuproptosis inhibitor TTM. Res reduced glucose uptake, lactate production, ATP generation, and downregulated GLUT1, HK2, LDHA, and PKM2, thereby suppressing aerobic glycolysis-a process reversed by PFKFB3 overexpression. Furthermore, Res inhibited PI3K and AKT phosphorylation; the PI3K activator 740 Y-P counteracted Res-mediated effects while the PI3K inhibitor LY294002 enhanced them. In vivo experiments confirmed that Res treatment markedly diminished tumor size and mass, lowered Ki-67 proliferation marker, enhanced programmed cell death, suppressed PI3K/AKT signaling, decreased glycolytic enzyme levels, and elevated copper-dependent cell death mediators. Res exerts anti-AML effects by inhibiting the PI3K/AKT pathway while coordinately regulating aerobic glycolysis and cuproptosis in AML cells. - Source: PubMed
Publication date: 2026/04/30
Lian ChengLiu YanhuiLei Pingchong