UCP3 Blocking Peptide (Rat)
- Known as:
- UCP3 Blocking Peptide (Rat)
- Catalog number:
- 30r-au003
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- UCP3 Blocking Peptide (Rat)
Related genes to: UCP3 Blocking Peptide (Rat)
- Gene:
- UCP3 NIH gene
- Name:
- uncoupling protein 3
- Previous symbol:
- -
- Synonyms:
- SLC25A9
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-11
- Date modifiied:
- 2016-04-28
Related products to: UCP3 Blocking Peptide (Rat)
α - Calcitonin Gene Related Peptide, α - CGRP, rat&_945;2&_946;1 Integrin Ligand Peptide&_946;_catenin peptide'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(2_Furoyl)_PAR_2 (2_6)_Orn amide (mouse, rat) Salt Trifluoroacetate Binding _ Synonym (2_Furoyl)_LIGRLOamide SumFormula C36H63N11O8(2_Furoyl)_PAR_2 (2_6)_Orn amide (mouse, rat) Salt Trifluoroacetate Binding _ Synonym (2_Furoyl)_LIGRLOamide SumFormula C36H63N11O8(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala13)-Apelin-13 (human, bovine, mouse, rat) 98% C63H107N23O16S CAS: 568565-11-7(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala92)-Peptide 6 98% C93H155N31O26 CAS:(Ala96)-Myelin Basic Protein (87-99) (human, bovine, rat) 98% C70H110N20O17 CAS:(Ala96)_Myelin Basic Protein (87_99) (human, bovine, rat) Salt _ Binding _ Synonym SumFormula C72H112N20O17 Related articles to: UCP3 Blocking Peptide (Rat)
- Main risk factors associated with the development of sarcopenia (coexistence of muscle mass loss and dysfunction) are a sedentary lifestyle coupled with obesity. Associated mitochondrial dysfunction leads to energy deficits and perturbations in the balance between protein synthesis and degradation, thereby triggering muscle dysfunction or atrophy. Aside from exercise, which is challenging to implement and maintain, particularly in women, treatments for diminishing sarcopenia are scarce. The objective of the present study was to evaluate the effect of the flavanol (-)-epicatechin (EC) in a hypercaloric diet-induced obese female rat model. Muscle strength and endurance, as well as relative mitochondrial DNA content in skeletal muscle, were assessed. - Source: PubMed
Publication date: 2026/03/22
Herrera-Cogco Elena de la CHerrera-Meza SocorroMartínez-Meza YuridiaPérez-Durán JavierCeballos GuillermoMéndez-Bolaina EnriqueNájera Nayelli - Cisplatin is an effective chemotherapeutic agent, yet its clinical utility is limited by dose-dependent nephrotoxicity. Alpha-1 antitrypsin (AAT) has cytoprotective, anti-inflammatory, and antiapoptotic properties, but its therapeutic potential in cisplatin-induced acute kidney injury (AKI) remains unclear. A murine cisplatin-AKI model was used to evaluate whether AAT (80 mg/kg) ameliorates renal injury. Renal function, oxidative stress, NADPH oxidase (NOX) isoforms, mitochondrial metabolism, inflammatory mediators, apoptosis, and fibrosis-related markers were assessed using biochemical, histological, immunohistochemical, and Western blot analyses. Cisplatin markedly impaired renal function and induced tubular injury; meanwhile, AAT significantly reversed these changes. Cisplatin also induced severe oxidative stress and disrupted the balance of NOX isoforms; AAT restored redox homeostasis. Cisplatin upregulated CPT1A/PDK4 and suppressed CPT2, UCP3, PGC1α, and DRP1, inducing maladaptive mitochondrial changes, indicating impaired β-oxidation and defective mitochondrial dynamics; AAT reversed these alterations, restoring normal mitochondrial metabolism. IL-1β, IL-6R, OPN, and F4/80 expression, recovery of the Bax/Bcl-2 ratio, and MAPK activation were reduced, indicating decreased inflammation and apoptosis; profibrotic markers were also reduced. AAT confers multifaceted protection against cisplatin-induced AKI by restoring redox balance, mitochondrial homeostasis, and inflammatory and apoptotic signaling. These findings support AAT as a promising therapeutic agent for preventing cisplatin nephrotoxicity. - Source: PubMed
Publication date: 2026/02/02
Kim MinaOh Se-HyunHan JinAhn Ji-SunOh Eun-JooJung Hee-YeonChoi Ji-YoungCho Jang-HeePark Sun-HeeKim Chan-DuckKim Yong-LimJeon You HyunLim Jeong-Hoon - With the ongoing upgrade in consumption patterns, the pork market is shifting from a focus on quantity to an emphasis on quality, demanding higher intramuscular fat content alongside maintained growth rates. Crossbreeding between the Chinese lean-type Songliao black pig and the high-quality local breed Leixiang pig allows rapid integration of parental superior traits, resulting in hybrid vigor that effectively improves pork quality, growth performance, and economic benefits. We conducted transcriptomic and 4D microDIA proteomic sequencing analyses on the muscle tissue from hybrid offspring of purebred Songliao black pigs and Songliao × Leixiang black pigs. Extensive phenotypic analyses were performed on Songliao black pigs and Songlei black pigs using multiple trait indicators. Six pigs were selected and categorized into relatively high and low intramuscular fat groups. Integrated analysis of transcriptomic and proteomic data identified candidate genes within significantly annotated lipid-related pathways via KEGG, including , , , , , , , and . Among these, was significantly associated with fatty acid metabolism pathways. By analyzing all significantly differential genes and proteins, six candidate genes were identified as key determinants of genetic variation in lipid deposition: , , , , , and . This preliminary exploratory multi-omics study provides a valuable resource for probing intramuscular fat deposition, aiming to support pork-trait improvement in breeding and to establish a fresh theoretical basis for clarifying the molecular mechanisms of meat-quality heterosis in Songlei black pigs. - Source: PubMed
Publication date: 2026/01/29
Zhang YunpengZhang QiKumar Suthar TeerathXu JingXie YupengWang ZhihaoSun Wu-ShengPan LiZhao YuanZhang Shu-Min - The rising incidence of cancer has demanded the development of new anti-cancer chemical sources. The presence of phenolics in hazelnut cell cultures has led to the development of new and potential pharmacotherapeutic uses. Hazelnut extract has emerged as a promising candidate due to its high phytochemical content. HCT-116 colorectal cancer IC cell viability of Palaz and Tombul hazelnut extracts was determined as 400 μg/mL and 200 μg/mL, respectively. Flow cytometry annexin V-fluorescein isothiocyante (FITC) apoptosis detection indicated apoptosis of Tombul hazelnut extract and Palaz hazelnut extract as 23.53% and 17.47%, respectively. The apoptosis result of flow cytometry was also supported at the protein level. Hazelnut extracts resulted in an increased loss of MMP as well. The loss of MMP has significantly increased from an average of 0.61% to 16.17% in Tombul hazelnut extract and to 20.38% in Palaz hazelnut extract. This is further supported by screening , and gene expressions. Targeting apoptosis pathways, particularly MMP, is an effective strategy for cancer prevention and treatment. Hazelnut extract contains phenolic compounds, which activate these pathways, resulting in enhanced apoptosis in colorectal cancer cells. The phenolic contents of Palaz and Tombul hazelnut extracts were determined as 271.72 ± 5.3 mg gallic acid equivalent (GAE)/100 g sample dry weight (DW) and 85.23 ± 2.2 mg GAE/100 g sample DW, respectively. Further, hazelnut extract may reduce oxidative stress, contributing to its anti-cancer properties. The extracts could be utilized as functional ingredients in foods and nutraceuticals to assist with cancer prevention and treatment. - Source: PubMed
Publication date: 2025/12/19
Bayram BanuDemircan EvrenKarimidastjerd AtefehAkyüz Elvan YılmazTutar Yusuf - Wnt and its crosstalk signaling pathways are involved in the modulating ischemia‒reperfusion (I/R) injury. However, whether Wnt2 is a novel therapeutic agent for I/R injury is largely unknown. Here, we show that the downregulation of serum Wnt2 levels in acute myocardial infarction (AMI) patients following reperfusion therapy, and Wnt2 levels are inversely correlated with the levels of myocardial injury markers (cTnT and CK-MB). Therapeutic administration of recombinant Wnt2 protein (rbWnt2) alleviates cardiac I/R injury and improves cardiac function by suppressing ROS levels and cardiomyocyte death in mice. Further analysis revealed that rbWnt2 downregulated Nap1L1 to reactivate the transcription of antioxidant genes (SOD, GPX, and UCP3) to reduce ROS levels and subsequently inhibit cardiomyocyte apoptosis and ferroptosis during the I/R process. Cardiac-specific Nap1L1 knockdown attenuated I/R injury, whereas overexpression of Nap1L1 partly abolished the cardiac protection mediated by rbWnt2 administration in the I/R model. Mechanistically, Wnt2 promoted Nap1L1 ubiquitination and degradation to restore ROS scavenging systems via Lrp6-mediated recruitment of the E3 ligase Trim11 in I/R hearts. Nap1L1 suppression plays a critical role in mediating the cardioprotective effects of rbWnt2. These findings establish Wnt2 as a therapeutic agent that targets compartmentalized oxidative damage, suggesting a novel strategy to mitigate I/R injury through the Lrp6/Trim11/Nap1L1 axis. - Source: PubMed
Publication date: 2025/12/16
Wang YingChen LimingLin JinyiLiu XiJin KejiaHuang ChenxingWang HaoJia JianguoWu JianDing ZhiwenGao PanGe JunboGong HuiZou Yunzeng