Ask about this productRelated genes to: UCP2 antibody
- 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 antibody
Related articles to: UCP2 antibody
- 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 - Hepatic encephalopathy (HE) is a severe clinical condition with limited therapeutic options. Silybin, a principal bioactive constituent of milk thistle, is a natural compound known for its protective effects against various liver diseases and neurodegenerative disorders. Silibinin meglumine (SM), the meglumine salt of silybin, is widely used in the management of hepatic disorders. However, the therapeutic potential and mechanistic basis of SM in HE remain incompletely elucidated. In this study, SM reduced serum ammonia levels and improved hepatic function markers, including alanine transaminase, aspartate transaminase, and total bilirubin (TBil), in thioacetamide (TAA)-induced HE mice. SM also attenuated inflammatory cytokines such as tumor necrosis factor (TNF) and interleukin-6 (IL-6) in both plasma and brain tissue, reduced the oxidative stress marker malondialdehyde, and increased glutathione levels. Furthermore, molecular docking, cellular thermal shift assay (CETSA), drug affinity responsive target stability (DARTS) assay, and microscale thermophoresis (MST) assay collectively indicated that uncoupling protein 2 (UCP2) may serve as a direct molecular target of SM in mitigating HE. Notably, SM downregulated UCP2 expression in liver tissue and alleviated oxidative stress and mitochondrial dysfunction through modulation of the UCP2/PINK1/Drp1/mitofusin-2 (MFN2)/LC3B pathway. Additionally, co-administration of a UCP2 inhibitor partially attenuated the antioxidant effects of SM; however, no statistically significant reduction was observed in alanine aminotransferase (ALT) and aspartate aminotransferase (AST). In summary, this study demonstrates that SM-mediated targeting of UCP2 enhances hepatic mitochondrial function and suppresses excessive mitophagy, thereby ameliorating TBil in TAA-induced HE. These findings suggest that SM may represent a promising therapeutic strategy for TAA-induced HE. - Source: PubMed
Li YueChen HongChen XinyiZhou ZhangqiuWang JiemanZhang YuanyuanZhang ShengpengHe HongliangKou Junping - -Aminobutyric acid (GABA) is the principal inhibitory neurotransmitter in the central nervous system and is involved in the development of neural tissue as well as the regulation of its functions. Meanwhile, GABA has also been demonstrated to confer multiple physiological benefits, including alleviating stress and improving metabolic homeostasis. This study investigated GABA effects on proliferation, differentiation, and temperature stress protection of bovine skeletal muscle satellite cells (BSCs). - Source: PubMed
Publication date: 2026/04/14
Manzoor AbidNaseem SajidaFu ZhiqiRuan ChaohuiLiu XuYan ChunriChoi SeonghoLi Xiangzi