Anti-UCP1 polyclonal antibody (DPABH-26313)

Rabbit anti-Human UCP1 (N-terminal) polyclonal antibody for ICC/IF, WB, IHC-P


Host Species
Antibody Isotype
Species Reactivity
Mouse, Rat, Spermophilus tridecemlineatus
Synthetic peptide conjugated to KLH, corresponding to amino acids 145-159 of Human UCP1, with N-terminal cysteine added.


Application Notes
ICC/IF: 1/500; WB: 1/1000; IHC-P: 1/500.
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.


Alternative Names
UCP1; uncoupling protein 1 (mitochondrial, proton carrier); UCP; mitochondrial brown fat uncoupling protein 1; SLC25A7; thermogenin
Entrez Gene ID
UniProt ID

Product Background

Adipogenesis; Electron Transport Chain; Huntingtons disease; Metabolism; Mitochondrial Uncoupling Proteins; PPAR signaling pathway;


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We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More

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Anti-Obesity Effect of Standardized Extract of Microalga Phaeodactylum tricornutum Containing Fucoxanthin


Authors: Koo, Song Yi; Hwang, Ji-Hyun; Yang, Seung-Hoon; Um, Jae-In; Hong, Kwang Won; Kang, Kyungsu; Pan, Cheol-Ho; Hwang, Keum Taek; Kim, Sang Min

Fucoxanthin (FX), a marine carotenoid found in macroalgae and microalgae, exhibits several beneficial effects to health. The anti-obesity activity of FX is well documented, but FX has not been mass-produced or applied extensively or commercially because of limited availability of raw materials and complex extraction techniques. In this study, we investigated the anti-obesity effect of standardized FX powder (Phaeodactylum extract (PE)) developed from microalga Phaeodactylum tricornutum as a commercial functional food. The effects of PE on adipogenesis inhibition in 3T3-L1 adipocytes and anti-obesity in high-fat diet (HFD)-fed C57BL/6J mice were evaluated. PE and FX dose-dependently decreased intracellular lipid contents in adipocytes without cytotoxicity. In HFD-fed obese mice, PE supplementation for six weeks decreased body weight, organ weight, and adipocyte size. In the serum parameter analysis, the PE-treated groups showed attenuation of lipid metabolism dysfunction and liver damage induced by HFD. In the liver, uncoupling protein-1 (UCP1) upregulation and peroxisome proliferator activated receptor (PPAR) downregulation were detected in the PE-treated groups. Additionally, micro computed tomography revealed lower fat accumulation in PE-treated groups compared to that in the HFD group. These results indicate that PE exerts anti-obesity effects by inhibiting adipocytic lipogenesis, inducing fat mass reduction and decreasing intracellular lipid content, adipocyte size, and adipose weight.

Melanocortin 4 receptor-mediated effects of amylin on thermogenesis and regulation of food intake


Authors: Li, Xiaojing; Fan, Kuikui; Li, Qiang; Pan, Deng; Hai, Rihan; Du, Chenguang

Aims: Amylin, a pancreatic hormone cosecreted with insulin, exerts important anorexic and weight-loss effects. Melanocortin 4 receptor (MC4R) signalling plays a critical role in energy homeostasis; however, its role on amylin-dependent regulation of food intake and adaptive thermogenesis of interscapular brown adipose tissue (IBAT) are unclear. In this study, we examined the effects of amylin on food intake and thermogenesis on IBAT via the MC4R pathway in mice. Materials and methods: Acute food consumption and thermogenesis in IBAT were measured in male wild-type (WT) and MC4R-deficient mice following intraperitoneal injection of amylin and SHU9119, an MC3R/4R antagonist, to determine the role of the central melanocortin system on the hypothalamus and IBAT. Results: Amylin (50 mu g/kg) suppressed feeding and stimulated thermogenesis on IBAT via activation of the MC4R system in mice. Pharmacological blockade of MC4R using SHU9119 (50 mu g/kg) attenuated amylin-induced inhibition of feeding and stimulation of thermogenesis in IBAT. No changes were observed when SHU9119 was injected alone. Moreover, amylin significantly increased MC4R expression and c-Fos neuronal signals in the arcuate nucleus and significantly increased acetyl-CoA carboxylase (ACC) phosphorylation in the hypothalamus and IBAT and uncoupling protein-1 (UCP1) expression in the IBAT of WT mice via the MC4R pathway. Conclusion: The melanocortin system was involved in amylin-induced suppression of food intake and activation of thermogenesis in both the hypothalamus and IBAT via modulation of ACC phosphorylation and UCP1 expression.

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