Recombinant Human Dihydrolipoamide S-Acetyltransferase DLAT
- Known as:
- Recombinant Human Dihydrolipoamide S-Acetyltransferase DLAT
- Catalog number:
- enz-082
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- Recombinant Human Dihydrolipoamide S-Acetyltransferase DLAT
Related genes to: Recombinant Human Dihydrolipoamide S-Acetyltransferase 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: Recombinant Human Dihydrolipoamide S-Acetyltransferase DLAT
Related articles to: Recombinant Human Dihydrolipoamide S-Acetyltransferase DLAT
- Mitochondria-lysosome contacts regulates metabolic reprogramming in cancer, yet its role in glioblastoma pathogenesis remains poorly defined. - Source: PubMed
Publication date: 2026/04/21
Huang YanpingSu DongyuanCui XiaotengDing YaqingZhan QiHong BiaoZhao JixingXu HanyiCui LongtaoCheng ChunchaoJu JiashengWang QixueWang YunfeiYang EryanYi KaikaiPeng DazhaoHu HuiminKang Chunsheng - Excessive advanced glycation end products (AGEs) can lead to cardiovascular diseases such as myocardial fibrosis (MF). Although studies have found that AGEs induce cuproptosis, and cuproptosis promotes fibrosis, it has not been confirmed whether AGEs promote MF through cuproptosis. AGEs increased intracellular copper levels, promoted the expression of solute carrier family 31 member 1 (SLC31A1), and downregulated the expression of ferredoxin 1 (FDX1), lipoic acid synthetase (LIAS), lipoylated (Lip)-dihydrolipoamide S-succinyltransferase (DLST), and Lip-dihydrolipoamide S-acetyltransferase (DLAT) in cardiac fibroblasts (CFs). All of these key cuproptosis regulatory gene expression abnormalities indicate that cuproptosis is induced. AGEs also decreased adenosine triphosphate content and inhibited the activities of mitochondrial complexes I and III, but these regulatory effects were significantly weakened after SLC31A1 downregulation. Meanwhile, AGEs significantly promoted the expression of alpha smooth muscle actin, collagen I, collagen III, and transforming growth factor-β1, while SLC31A1 siRNA or copper chelator ammonium tetrathiomolybdate (TTM) blocked these promoting effects. Similarly, CuCl also induced fibrosis gene expression, while SLC31A1 overexpression (SLC31A1-O) further enhanced these effects, but TTM reduced CF activation induced by CuCl plus SLC31A1-O. In addition, AGEs significantly promoted cell migration and enhanced the expression and secretion of matrix metalloproteinase (MMP)-2 and MMP-9, while SLC31A1 siRNA or TTM weakened these effects. SLC31A1-O plus copper treatment also had similar effects to AGEs, and these effects could also be blocked by TTM. Therefore, AGEs enhance copper transport by promoting SLC31A1 expression, which leads to intracellular copper overload and then induces cuproptosis, and finally promotes CF activation and migration. - Source: PubMed
Publication date: 2026/04/20
Xiao JianShi Zan-HuaMa Xin-HuaXu Dao-MiaoMing Guang-Feng - Colorectal cancer (CRC) remains a leading cause of cancer-related mortality, with limited therapeutic options for advanced-stage patients. Here, we identify DLAT, a key enzyme in mitochondrial metabolism, as a critical driver of CRC progression. Multi-omics analyses revealed that DLAT was overexpressed in CRC tissues and correlated with poor patient prognosis. The results showed that DLAT promoted CRC growth by promoting the resistance to mitochondrial antioxidant stress and suppressing ferroptosis. Mechanistically, DLAT directly bond to the mitochondrial glutathione (mtGSH) transporter SLC25A39 and enhanced its protein stability independent of intracellular GSH levels, leading to the maintain of mitochondrial GSH (mtGSH) import and redox homeostasis. Knockdown of DLAT or SLC25A39 disrupted mtGSH transport, elevated lipid peroxidation, and sensitized CRC cells to ferroptosis. We further identified a small molecular drug GL-V9 as a DLAT degrader. GL-V9 bond to DLAT and induced DLAT degradation through ubiquitin-proteasome pathway. The disruption of DLAT-SLC25A39 axis by GL-V9 led to mtGSH depletion and oxidative stress, as well as the significant suppression of CRC growth. These findings establish DLAT as a metabolic vulnerability in CRC and highlight GL-V9 as a promising therapeutic agent. - Source: PubMed
Publication date: 2026/04/18
Zhang KunZhang XinHuang ChenqiYang JunyiDong LongxuanChen XijingXun ChenGuo Yongjian - Lymph node metastasis, critically dependent on evasion of cancer cell death, drives poor prognosis in oral squamous cell carcinoma (OSCC). Through CRISPR-Cas9 screening in OSCC cell lines with divergent metastatic potential, we identified follistatin-like 3 (FSTL3) as a master regulator of lymph node metastasis. knockdown drastically suppressed metastasis. Mechanistically, FSTL3 loss induced cuproptosis susceptibility by suppressing SLC25A10, triggering mitochondrial succinate accumulation. Succinate promoted succinylation and upregulation of dihydrolipoamide S-acetyltransferase (DLAT), essential for cuproptosis execution, thereby crippling metastatic spread. Crucially, FSTL3 simultaneously orchestrates an immunosuppressive tumor microenvironment. FSTL3 recruits erythroid progenitor cells (EPCs) into tumor sites by upregulating CCR5 on EPCs. Concurrently, FSTL3-exposed EPCs exhibited elevated CD73 and PD-L1, establishing an immunosuppressive niche that promotes metastasis. Consequently, depletion in immunotherapy-resistant tumors unleashed potent antitumor immunity and synergized with immunotherapy. Our findings establish FSTL3 as a pivotal node coordinating dual metastasis mechanisms: cuproptosis resistance and immune evasion. Targeting FSTL3 disrupts both adaptive programs, effectively inhibiting lymph node metastasis. This work nominates FSTL3 as a therapeutic target; combining FSTL3 inhibition with immunotherapy represents a promising dual-targeting strategy to improve OSCC outcomes by simultaneously disabling cancer cell survival and immune escape. - Source: PubMed
Publication date: 2026/04/17
Li S-RWu Z-ZWang W-DMo W-TWang QYang E-LWang W-YYang Q-CLi HWu T-FSun Z-J - - Source: PubMed
Publication date: 2026/04/02
Li LinZhao HongjingNiu XiaopingLiu Pengwei