UCP2 Cell Transient Overexpression Lysate(Denatured)
- Known as:
- UCP2 Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00007351-T03
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- UCP2 Cell Transient Overexpression Lysate(Denatured)
Related genes to: UCP2 Cell Transient Overexpression Lysate(Denatured)
- Gene:
- UCP2 NIH gene
- Name:
- uncoupling protein 2
- Previous symbol:
- BMIQ4
- Synonyms:
- SLC25A8
- Chromosome:
- 11q13
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-11
- Date modifiied:
- 2016-04-28
Related products to: UCP2 Cell Transient Overexpression Lysate(Denatured)
Related articles to: UCP2 Cell Transient Overexpression Lysate(Denatured)
- Myocardial infarction causes persistent mitochondrial and metabolic dysfunction that drives adverse cardiac remodeling. Here we develop NAD-genipin nanomedicine for metabolic balance (NGB), a physiologically adaptive nanomedicine with staged intracellular release. In a mouse myocardial infarction model, NGB preferentially accumulates in ischemic myocardium, rapidly replenishes nicotinamide adenine dinucleotide (NAD) and subsequently provides mitochondria-associated sustained NAD-genipin exposure. This phase-linked delivery limits early mitochondrial stress, apoptosis and inflammation and later restores coordination between oxidative phosphorylation, glycolysis and fatty-acid utilization. Mechanistically, NGB supports sirtuin-1-associated oxidative metabolism and suppresses sustained upregulation of the mitochondrial uncoupling protein 2 (UCP2). In hypoxic cardiomyocytes, UCP2 knockdown plus NAD supplementation partially reproduces the NGB metabolic phenotype, whereas UCP2 overexpression and sirtuin 1 inhibition reverse distinct components of NGB-mediated respiratory and glycolytic recovery. NGB thereby reduces fibrosis and ventricular remodeling and preserves cardiac function, supporting temporally coordinated metabolic intervention after myocardial infarction. - Source: PubMed
Publication date: 2026/09/22
Wang JueXia YingciZheng WenxuanYuan WenqinHuang YunyingZhang YuntaoHuang QiongAi Kelong - Articular cartilage degeneration is a hallmark of osteoarthritis (OA); however, underlying molecular mechanisms remain poorly understood. Transforming growth factor alpha (TGFα) and chondrocyte metabolism have been independently implicated in OA pathogenesis; in this study, we investigated whether TGFα affects chondrocyte metabolism. - Source: PubMed
Publication date: 2026/09/02
White Emily LDay Emily AAppleton C ThomasGrol Matthew WBeier Frank - Hypoxia has therapeutic potential, but global hypoxia is toxic. Inducing safe, cell-specific hypoxia remains a clinically unmet need. We hypothesized that small-molecule-augmented oxygen consumption in adjacent cells induces neuron-specific hypoxia, representing a safe ischemic stroke strategy that mimics neural-directed developmental neovascularization. Using single-cell sequencing, a hypoxic probe, and knockout mice, we showed that ADT-OH (an active metabolite of a hepatoprotective drug) targeted sulfide-quinone oxidoreductase (SQR) to increase aerobic respiration in microglia/macrophages, thereby generating neuron-specific hypoxia after cerebral ischemia. Neuronal hypoxia promoted functional angiogenesis by specifically stabilizing hypoxia-inducible factor to upregulate the expression of neuron-derived vascular endothelial growth factor, supporting a neural-directed angiogenic mechanism. ADT-OH also restored the blood-brain barrier (BBB) via microglial/macrophage SQR. Notably, microglia/macrophage UCP2, the downstream mediator of SQR, was required for ADT-OH-induced BBB repair but not angiogenesis. Mechanistically, ADT-OH targeted UCP2 to increase Wnt/β-catenin signaling, which has been shown to mediate developmental BBB formation. In summary, one small molecule targeting SQR achieves therapeutic cell-specific hypoxia. - Source: PubMed
Publication date: 2026/09/17
Wang Xiao-YingHuang Zi-YinHan RuiLi Xin-YuSong Yan-MeiWang QiXu Fu-YouZhu Zi-HuiCheng RongWu Hao-YuXia Yi-QingRen Hai-GangPan Xiao-FanXiao Guo-DongCheng JianJia Jia - Glutamate metabolism is crucial for intestinal epithelial metabolism, but its availability is limited in the hindgut. We used a hindgut-targeted delivery system to deliver L-glutamate and its metabolite α-ketoglutarate (AKG) to investigate the effects of glutamate metabolites on broiler growth and to reveal the potential underlying mechanism. In a three-week feeding trial, fifty-four broilers were randomly divided into three treatments, basal diet (control), basal diet supplemented with 0.1 % L-glutamate (L-Glu) pellets and basal diet supplemented with 0.1 % AKG pellets. The growth performance, intestinal health, microbiota and ammonia nitrogen metabolism were examined. Then, RNA sequencing was adopted to reveal transcriptomic profile of cecal mucosal epithelial cells. Finally, the potential mechanism of AKG in regulating intestinal redox homeostasis was also investigated by in vitro cell model. The results demonstrated that hindgut-targeted delivery of AKG significantly increased average daily gain and decreased the feed-to-gain ratio (F/G), which is better than the effect of L-Glu. Although AKG did not significantly affect intestinal barrier function, inflammation, or microbiota composition, it markedly reduced serum levels of phenylalanine, tryptophan and valine, while significantly reduced ammonia content in cecal contents. Transcriptomic sequencing showed that AKG significantly downregulated oxidative phosphorylation (OXPHOS) in the cecal mucosa and reduced oxidative damage. In vitro experiments confirmed that AKG significantly reduced OXPHOS and alleviated oxidative damage in colonocytes. Further, cellular thermal shift assay (CETSA) and pharmacological study revealed that uncoupling protein 2 (UCP2) mediated the effect of AKG on redox status of colonocytes. Thus, hindgut-targeted delivery of AKG enhances broiler growth performance by activating UCP2 in intestinal epithelial cells, reducing OXPHOS and alleviating oxidative damage in the intestinal mucosa. These findings support precise strategies for regulating growth in poultry production. - Source: PubMed
Publication date: 2026/07/14
Yang XueFeng XiaohuaHuang WeiGan XinyuJiang HongfengZhu YunlongWang YujunLi GenghuiPeng XiaofengRong JingWu RuifanZhu CanjunWang LinaWang SongboJiang QingyanShu Gang - Adults born with intrauterine growth restriction (IUGR) are at a significantly increased risk of developing metabolic syndrome. Postnatal nutritional patterns are critical modifiers of this risk. This study investigated the effects of different perinatal nutritional interventions on glucose/lipid metabolism and hepatic steatosis in IUGR offspring, and explored the role of hepatic uncoupling protein 2 (UCP2). - Source: PubMed
Publication date: 2026/08/31
Zeng QiongWu YixiChen YantingLi QingDeng ZhijianChen XiutongWang JingsaHe YitingMa ZemingYang RunjiaLin Kun