UCP2 Blocking Peptide (Mouse)
- Known as:
- UCP2 Blocking Peptide (Mouse)
- Catalog number:
- 30r-au001
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- UCP2 Blocking Peptide (Mouse)
Related genes to: UCP2 Blocking Peptide (Mouse)
- 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 Blocking Peptide (Mouse)
Related articles to: UCP2 Blocking Peptide (Mouse)
- The aim of this preliminary study was to determine the effect of taurine on the expression of genes involved in glycolysis, oxidative phosphorylation, inflammation, autophagy, and regenerative activity in cultured peripheral blood mononuclear cells (PBMCs) and articular cartilage explants from patients with end-stage rheumatoid arthritis (RA). PBMCs and knee articular cartilage were obtained from 20 patients with RA (3 men and 17 women) aged 62.2 ± 10.9 years, with a mean disease duration of 17.5 years (range: 2-43), prior to arthroplasty. PBMCs and cartilage explants were cultured in the presence of 50 µM taurine. Gene expression was determined using real-time reverse transcriptase polymerase chain reaction (RT-PCR). Protein expression of the examined genes in PBMCs was quantified using ELISA. In the presence of 50 µM taurine PBMCs from patients with RA demonstrated a significant increase in the expression of genes encoding pyruvate kinase (PKM2), succinate dehydrogenase (SDHB), uncoupler of oxidation and phosphorylation (UCP2), ATP synthase (ATP5B), and unc-51-like kinase 1 (ULK1). At the same time a significant decrease in tumor necrosis factor (TNF)α and interleukin (IL)-1β expression was noted. In cartilage explants, taurine upregulated SDHB, UCP2, ULK1, and type 2 collagen gene (COL2A1), and decreased TNFα expression. We concluded that, under in vitro conditions, taurine can influence the expression of genes involved in glycolysis, oxidative phosphorylation, inflammation, autophagy, and regenerative processes in PBMCs and articular chondrocytes from patients with end-stage RA. - Source: PubMed
Publication date: 2026/05/09
Tchetina ElenaKushnareva IrinaAnisimova EkaterinaVienozinskaite AngelePlastinina OksanaMakarov MaksimLila Aleksandr - Alzheimer's disease (AD) is associated with mitochondrial dysfunction and impaired energy metabolism in astrocytes. Although ghrelin is known to exert neuroprotective effects, the mechanisms through which it modulates astrocyte bioenergetics under AD-like conditions remain incompletely defined. In primary astrocytes treated with Aβ oligomers, ghrelin attenuated mitochondrial damage, reducing ROS and enhancing mitochondrial membrane potential (ΔΨm) and respiratory complex activities. Glycolytic function was partially restored, as evidenced by upregulation of key enzymes, increased glucose uptake, lactate release, and NAD/NADH ratio. Ghrelin inhibited autophagosome formation while enhancing mitophagy (increased LC3II/I and Parkin) and suppressed inflammation. In co-culture models, these metabolic improvements enhanced astrocytic support for neurons, reducing apoptosis and promoting neurite growth, an effect abolished by the glycolytic inhibitor 2-DG. Mechanistically, ghrelin upregulated uncoupling protein 2 (UCP2), which inhibited forkhead box protein O1 (FOXO1) nuclear translocation. In Aβ-injected mice with UCP2 or FOXO1 modulation, ghrelin improved cognitive performance and reduced pathology, effects that were negated by UCP2 knockdown and partially rescued by FOXO1 knockdown. In conclusion, ghrelin ameliorates Aβ-induced astrocyte dysfunction involving the UCP2-FOXO1 pathway, partially restoring mitochondrial integrity, glycolytic metabolism, and neurotrophic support, suggesting its therapeutic potential. - Source: PubMed
Publication date: 2026/05/25
Guo YaoxueWang XueyanZhang LixiangLiu XingLu PuLiang FuruWu JingZhao JunliHai Yan - A recent study reported that endothelial PAS domain protein 1 (EPAS1; hypoxia-inducible factor 2α) acts downstream of PGC-1α to regulate the slow-twitch muscle fiber program in mice, yet its role in human physiology and exercise adaptation remains unclear. The aim of this study was threefold: (1) to investigate EPAS1 gene expression in human skeletal muscle and its association with muscle fiber composition and the expression of endurance-related genes; (2) to determine how EPAS1 expression responds to aerobic training; and (3) to examine whether EPAS1 genetic variation is linked to aerobic capacity, hemoglobin, and athletic status. The study involved 1234 subjects, including 943 athletes and 291 untrained individuals. EPAS1 gene expression was significantly higher in endurance athletes compared with power athletes (p = 0.011) and was positively associated with the proportion of slow-twitch muscle fibers in the vastus lateralis of untrained subjects (p = 0.0008) and athletes (p = 0.0033). EPAS1 expression was higher in females (p = 0.0028) and negatively associated with smoking status (p = 0.0007). Moreover, EPAS1 expression showed positive association with endurance-related genes, including ANGPT2, CKM, CPT1B, EPOR, FNDC5, HIF1A, KDR, MYBPC3, NFATC4, NOS3, PPARA, PPARD, PPARGC1A, UCP2, and VEGFA. Analysis of 24 publicly available skeletal muscle transcriptomic datasets demonstrated that EPAS1 expression increased significantly (meta-analysis p = 9.2 × 10) following aerobic training. Finally, genetically predicted higher EPAS1 expression (i.e., carriage of the EPAS1 rs6756667 A allele) was positively associated with endurance athlete status in both sexes (p = 0.0004) and with VO₂max (p = 0.046) and hemoglobin (p = 0.041) in male athletes. These findings potentially identify EPAS1 as an important genetic factor associated with muscle fiber composition, endurance-related phenotypes, and adaptation to aerobic training. - Source: PubMed
Dautova Albina ZValeeva Elena VSemenova Ekaterina AMavliev Fanis AZverev Alexey ANazarenko Andrey SJohn GeorgeZhelankin Andrey VLarin Andrey KKulemin Nikolay ASultanov Rinat IGenerozov Edward VAhmetov Ildus I - Cancer cells rely upon fatty acids (FA) for proliferation, survival, and metastasis. Overexpression of long-chain acyl CoA synthetase 1 (ACSL1), responsible for long-chain FA synthesis, can increase cell invasion and proliferation. Uncoupling protein-2 (UCP2) promotes FA metabolism over glucose utilization in colorectal cancer cells. We aimed to investigate the association of 45bp ins/del and rs8086 polymorphisms with the clinicopathological characteristics in patients with colorectal cancer. The study included 183 patients with colorectal cancer, 110 (60.1%) men and 73 (39.9%) women, with an average age of 62.1 years. Clinicopathological characteristics: tumor location, histological differentiation, presence of lymph node metastases, presence of distant metastases, and stage of the disease were collected for all patients. Rs8086 polymorphism genotypes were detected by Real-time PCR using TaqMan SNP Genotyping assay, while genotyping of 45 bp ins/del polymorphism was performed using the PCR method. Distant metastases were more frequent in carriers of the TT genotype than carriers of the CC or CT genotype (p=0.046). Also, carriers of the 45 I allele (II+ID genotype) had distant metastases more frequently than patients with the DD genotype (p=0.029). It has also been observed that there is a statistically significant association of and genotype with cancer localization (p=0.006 and p=0.017, respectively). The results suggest that rs8086 and 45 bp ins/del polymorphisms are associated with the occurrence of distant metastases and tumor location in patients with colorectal cancer. - Source: PubMed
Publication date: 2026/05/14
Ajaj ECvetković DRašić MRistanović MPetrović Šunderić JDragutinović VMaksimović N - Genipin-crosslinked nanocarrier systems demonstrate enhanced physicochemical and therapeutic performance across multiple platforms, including nanoparticles, liposomes, hydrogels, nanogels, and lipid-based systems. These systems consistently achieve 25-35% amine crosslinking efficiency, resulting in improved structural stability, higher drug encapsulation efficiency, and sustained release profiles compared with non-crosslinked or synthetically crosslinked counterparts. Preclinical evidence indicates that approximately 25-35% of reported studies include in vivo validation, demonstrating prolonged systemic circulation, enhanced tumor accumulation, significant tumor growth inhibition, and reduced off-target toxicity. Mechanistically, genipin induces mitochondrial dysfunction via UCP2 inhibition, leading to elevated intracellular ROS levels, modulation of Bax/Bcl-2 balance, activation of caspase cascades, and suppression of NF-κB, PI3K/Akt/mTOR, and STAT3 signaling pathways. These effects collectively promote apoptosis, ferroptosis, anti-angiogenesis, and inhibition of metastasis. Integration of genipin into nanocarriers improves pharmacokinetic parameters, including increased half-life, enhanced bioavailability, and reduced systemic clearance, while enabling synergistic therapeutic strategies such as chemo-, gene-, and phototherapy. Compared with conventional crosslinkers, genipin exhibits markedly lower cytotoxicity and superior biocompatibility, supporting higher cell viability and reduced inflammatory responses. However, challenges remain, including slower crosslinking kinetics, formulation variability, scalability limitations, and insufficient long-term in vivo safety data. Overall, genipin-based nanocarriers demonstrate significant potential as multifunctional platforms for improving the efficacy and safety of cancer therapy, though further translational and clinical validation is required. - Source: PubMed
Publication date: 2026/05/02
Sharma TanujKaur SimranjitSharma Jai BhartiWahab ShadmaKapoor Devesh U