Rat Dihydrolipoyl Transacetylase ELISA , DLAT
- Known as:
- Rat Dihydrolipoyl Transacetylase Enzyme-linked immunosorbent assay test , DLAT
- Catalog number:
- E02D0021
- Category:
- -
- Supplier:
- Blue Gene Biotech
- Gene target:
- Rat Dihydrolipoyl Transacetylase ELISA DLAT
Related genes to: Rat 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: Rat Dihydrolipoyl Transacetylase ELISA , DLAT
Related articles to: Rat Dihydrolipoyl Transacetylase ELISA , DLAT
- Tanshinone IIA (TSA) is the core liposoluble active component of Salvia miltiorrhiza, a traditional Chinese medicine, and exhibits multiple pharmacological activities including anti-inflammation, anti-oxidation, anti-apoptosis and mitochondrial function improvement. Studies have confirmed that TSA can ameliorate cognitive function in rats with vascular dementia (VaD) by alleviating cerebral ischemic injury, inhibiting neuroinflammation, protecting the blood-brain barrier and other pathways. However, it has not been reported whether TSA exerts its neuroprotective effect by regulating the cuproptosis pathway. Focusing on cuproptosis, this study investigated the effects of TSA on cognitive impairment, neuronal injury and cuproptosis-related mechanisms in a rat model of VaD. - Source: PubMed
Publication date: 2026/08/24
Lv HongxiaoYang XinyuLiu YutongZhou JunweiYu Wentao - In response to the high metabolic resilience and immunosuppression characteristic of triple-negative breast cancer, this study established a CuGaO (CGO) nano sonocatalytic platform to reshape the therapeutic landscape through a metabolic hijacking dual death cascade strategy. The ultrasound activates CGO to generate reactive oxygen species (ROS), and facilitates the release of Cu and Ga in tumor. The Ga precisely disrupts iron metabolism and suppresses the expression of Fe-S cluster proteins via the metal mimicry effect, thereby achieving metabolic disarmament at a fundamental level. The decrease of Fe-S proteins, along with Cu-induced dihydrolipoamide S-acetyltransferase (DLAT) oligomerization, results in dual protein toxicity, causing mitochondrial impairment and triggering efficient cuproptosis. ROS further directly damage mitochondria, leading to a reduction in ATP production. The consequent ion pump failure, coupled with oxidative stress, precisely triggers the caspase-1-mediated pyroptosis pathway. The inflammatory explosion interwoven with cuproptosis and pyroptosis, significantly amplifies cellular damage and promotes the release of immunogenic signals. In vivo results show that the system not only inhibits primary tumor growth, but also makes macrophages become a pro-inflammatory type, and increases CD8 T cell infiltration, so it inhibits distant metastatic lesions. This cascade strategy offers a novel synergistic approach to overcoming metabolic resistance and metastasis in refractory tumors. - Source: PubMed
Publication date: 2026/08/19
Luo RuixinDong LileChen AihongHu JunyiWang ShijieZhu XiaofengWang KaiyangLu JieYin XueboLuo YuJiang FengLiu Xijian - Intra- and intertumoral heterogeneities raise fundamental biological questions and have important implications for accurate cancer diagnosis, prognosis, and treatment. These heterogeneities reflect tumor complexity, including a pronounced diversity in metabolic phenotypes and profiles. This study demonstrates that in vivo deuterium metabolic imaging (DMI) data acquired with sufficiently high spatiotemporal resolution provide a minimally invasive approach to assess these heterogeneities. A multifrequency DMI approach was used to examine tumor heterogeneities within and between colon cancer models. Regions of high and low glucose enrichment and labeled lactate accumulation could thus be detected; these were analyzed using unsupervised clustering strategies based on -means clustering of area-under-the-curve information, and principal components analysis with Gaussian mixture modeling. Spatial alignment of these imaging-derived clusters for H-glucose and H-lactate showed good agreement with each other as well as with histological sections, validating the biological relevance of the identified subregions. Immunohistochemical analyses showed that glucose-enriched subregions were positively correlated with the expression of GLUT1 and DLAT, while lactate-enriched areas showed elevated expression of LDHA and MCT4. These results demonstrate that in vivo DMI can distinguish metabolically distinct subregions within viable tumors and between tumor models. DMI-based metabolic maps could thus provide the means to characterize intra- and intertumoral heterogeneities, paving the way for imaging-based metabolic phenotyping in precision oncology. - Source: PubMed
Publication date: 2026/08/21
Liu XinjieWang SufeiZhao JinruiWang ShaShaSun PengZhou XinLiu MailiLiu ChaoyangFrydman LucioBao Qingjia - Sarcopenia is an age-related muscle wasting condition that currently lacks specific diagnostic biomarkers and effective treatments. This study aimed to identify mitochondria-related biomarkers for sarcopenia via integrated multi-omics. - Source: PubMed
Publication date: 2026/08/03
Wang ShengweiWu WeigenYin HuaChen QiushuoZhang LingHe Wen - Alzheimer's disease (AD) is a neurodegenerative disorder characterized primarily by progressive cognitive impairment, whose pathogenesis involves multiple pathological processes including protein deposition, metal homeostasis dysregulation, oxidative stress, mitochondrial dysfunction, and neuroinflammation. In recent years, metabolism-related cell death modalities such as ferroptosis, cuproptosis, and disulfidptosis have gradually been recognized as potentially involved in neuronal damage in Alzheimer's disease. This review summarizes the fundamental mechanisms of ferroptosis, cuproptosis, and disulfidptosis, along with their research evidence in AD. Ferroptosis is primarily driven by iron imbalance, lipid peroxidation buildup, and impaired GPX4 defense. This process exhibits a bidirectional amplification loop with Aβ and tau pathologies. Cuproptosis contributes to neuronal damage through abnormal copper accumulation, FDX1-related mitochondrial protein lipoylation dysfunction, loss of iron-sulfur cluster proteins, and proteotoxic stress. Disulfidptosis links glucose metabolism disorders, insufficient reducing power, and actin cytoskeleton vulnerability, providing novel insights into metabolic stress and structural damage in AD. Furthermore, the three modes of cell death can undergo cross-regulation through the SLC7A11-NADPH-GSH/GPX4 axis, the FDX1-DLAT/DLST-iron-sulfur cluster axis, as well as upstream factors such as p53, NRF2, and AMPK. Metabolic cell death may constitute a critical pathological network in AD. Targeting these death pathways and their shared hubs is expected to provide new directions for disease stratification, biomarker development, and disease-modifying therapies. - Source: PubMed
Publication date: 2026/07/30
Ding ShuyuGuo ZihanJi HengyuHe Jinting