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anti-Human UCP1 Anticorps:
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Human Monoclonal UCP1 Primary Antibody pour FACS, ICC - ABIN5680445
Moisan, Lee, Zhang, Hudak, Meyer, Prummer, Zoffmann, Truong, Ebeling, Kiialainen, Gérard, Xia, Schinzel, Amrein, Cowan: White-to-brown metabolic conversion of human adipocytes by JAK inhibition. dans Nature cell biology 2016
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Human Polyclonal UCP1 Primary Antibody pour IF (p), IHC (p) - ABIN675413
Lu, Ji, Zhang, Zhang, Zhang, An, Liu, Zheng: Resistance to obesity by repression of VEGF gene expression through induction of brown-like adipocyte differentiation. dans Endocrinology 2012
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Human Polyclonal UCP1 Primary Antibody pour IHC, ELISA - ABIN251297
Liu, Singh, Choi, Lee, Keramati, Samuel, Lifton, Shulman, Mani: Low density lipoprotein (LDL) receptor-related protein 6 (LRP6) regulates body fat and glucose homeostasis by modulating nutrient sensing pathways and mitochondrial energy expenditure. dans The Journal of biological chemistry 2012
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Human Polyclonal UCP1 Primary Antibody pour ELISA, WB - ABIN547557
Ishigaki, Katagiri, Yamada, Ogihara, Imai, Uno, Hasegawa, Gao, Ishihara, Shimosegawa, Sakoda, Asano, Oka: Dissipating excess energy stored in the liver is a potential treatment strategy for diabetes associated with obesity. dans Diabetes 2005
AtUCP1 and AtUCP2 are the first reported mitochondrial carriers in Arabidopsis to transport aspartate and glutamate
The transcriptome of overexpressing plants revealed a broad induction of stress-responsive genes not strictly related to the mitochondrial antioxidant machinery, suggesting that overexpression of AtUCP1 imposes a strong stress response within the cell.
Foliar NO3 (-) assimilation was enhanced in both aox1a and ucp1 compared with the wild-type, suggesting that foliar NO3 (-) assimilation is probably driven by a decreased capacity of mAET and an increase in reductant within the cytosol.
Overexpression of UCP1 in the mitochondrial inner membrane induced increased uncoupling respiration, decreased reactive pxygen species accumulation under abiotic stresses, and diminished cellular ATP content.
The main physiological role of UCP1 in Arabidopsis leaves is related to maintaining the redox poise of the mitochondrial electron transport chain to facilitate photosynthetic metabolism. [AtUCP1]
Cys28 substitution reduced ATP inhibitory effect, while Tyr269Phe mutant exhibited 2.8-fold increase in sensitivity to ATP.
Data indicate that the abundance of uncoupling protein 1 (UCP1) was significantly reduced in the intrauterine growth restriction (IUGR) piglets.
An alignment with human UCP1 revealed that exons 3 to 5 were eliminated by a deletion in the pig sequence.
The rs1800592 and rs3811791 of UCP1 gene are associated with obesity in general and in the moderate obese group in particular. The associated UCP1 polymorphisms in the moderate-obese group may regulate the impaired energy metabolism which plays a significant role in the initial stages of obesity.
Results suggest that G-quadruplex structure is a potential target to regulate the expression of uncoupling protein 1 (UCP1).
Cellular and genetic evidence supported the regulation of UCP1 transcription by IRX3 as a direct mechanism on the browning program of white adipocytes.
Multiple regression analysis showed that age, male gender, body max index, presence of obesity, type-2-diabetes mellitus, hypertension and coronary artery disease and left ventricular ejection fraction were associated with the expression levels of UCP1, PGC1alpha and PRDM16 mRNA
Results found a specific fatty acids binding site that is functionally important to the H+ transport activity of UCP1-mediated flux.
MKK6 acts as a repressor of UCP1 expression, suggesting that its inhibition promotes adipose tissue browning and increases organismal energy expenditure.
determined transcriptional levels of UCP1 and UCP2 in peripheral blood mononuclear cells (PBMCs) from patients with metabolic disorders: type 2 diabetes, obesity and from healthy individuals.
We observed that clozapine but not six other antipsychotic drugs reprogrammed the gene expression pattern of differentiating human adipocytes ex vivo, leading to an elevated expression of the browning marker gene UCP1, more and smaller lipid droplets and more mitochondrial DNA than in the untreated white adipocytes.
The GG genotype of the UCP1-3826 A/G polymorphism appears to contribute to the onset of childhood obesity in Turkish children. The GG genotype of UCP1, together with the del/del genotype of the UCP2 polymorphism, may increase the risk of obesity with synergistic effects. The ins allele of the UCP2 exon 8 del/ins polymorphism may contribute to low HDL cholesterolemia.
TENM2 knockdown induces both UCP1 mRNA and protein expression upon adipogenic differentiation without affecting mitochondrial mass.
The role of UCP1 gene polymorphisms A-3826G, A-1766G, Met229Leu and Ala64Thr in susceptibility to obesity or metabolic syndrome was reviewed.
Haplotype-based interaction between the PPARGC1A and UCP1 genes is associated with impaired fasting glucose (IFG) or type 2 diabetes mellitus (T2DM) among the residents of Henan province, China. Individuals with the haplotype AAG (PPARGC1A gene) and CTCG (UCP1 gene) have increased susceptibility to IFG or T2DM, while those with haplotype AAG (PPARGC1A gene) and CTCA (UCP1 gene) have a lower risk of IFG or T2DM.
human and rodent Brown adipose tissue have similar UCP1 function per mitochondrion.
glucocorticoids increased isoprenaline-stimulated respiration and UCP-1 in human primary brown adipocytes.
These results reveal different characteristics in the biological actions between WAT and BAT in obese humans. Increased levels of IL6, UCP1 and SIRT1 in the BAT were associated with metabolic parameters improvements.
UCP1 dietary activation can alleviate obesity. (Review)
The molecular features of UCP1 support a conventional mitochondrial carrier-like mechanism. (Review)
The history of discovery of UCP1, the mitochondrial uncoupling protein of brown adipocyte, has been described. (Review)
Transcriptional regulation of the UCP1 protein in obesity and normal thermogenesis has been described. (Review)
The H+ transport mediated by UCP1 was shown to be electrophoretic with a linear relation to the membrane potential. (Review)
Study presents novel evidence for a negative regulation of ER stress signaling to Ucp1 expression via the suppression of activator PPARG in beige adipocytes.
results demonstrate that in addition to controlling the BAT response to extreme cold, betaAR signaling is necessary to maintain basal Ucp1 tone and to couple BAT circadian rhythmicity to the central clock.
we demonstrate that the effects of UCP1 deficiency in BAT are not restricted to mitochondrial uncoupling. We conclude that brown adipose tissue of UCP1-/- mice exhibits pro-inflammatory immune cell infiltration and perturbations in ER homeostasis and that this phenotype is driven by cold exposure rather than lipid accumulation.
these data support a model in which LP-induced FGF21 drives UCP1-dependent increases energy expenditure to influence metabolic but not thermogenic endpoints.
Our results establish the feasibility of minimally invasive UTMD gene-based therapy administration in SKM, to induce overexpression of ectopic mUCP-1 after delivery of the thermogenic BAT gene program, and describe systemic effects of this intervention on food intake, weight loss, and thermogenesis
effect of CREG1 on Ucp1 promoter activity was also stimulated by retinoic acid. These results strongly suggest that CREG1 plays an important role on the regulation of UCP1 expression and brown adipogenesis
In murine primary adipocytes, norepinephrine (NE)induced a higher expression of Ucp1 and Pgc1a than non-NE-treated cells, and pinolenic acid (PLA) augmented the NE effect.
This study highlights the novel mechanism of HDAC3-regulated Ucp1 expression during beta-adrenergic receptor stimulation.
These findings suggested that HDAC6 contributes to mitochondrial thermogenesis in brown adipose tissue by increasing UCP1 expression through cAMP-PKA signaling pathway.
Findings demonstrated that one bout of both uphill and downhill exercise trainings as well as 8 weeks of training could increase the expression of PGC-1alpha and FNDC5 genes in the muscle tissues and the UCP1 gene in the subcutaneous adipose tissue.
To identify putatively causal regulators, we performed transcription factor binding site overrepresentation analyses in active chromatin regions and prioritized factors based on their expression correlation with the bona-fide brown adipogenic marker Ucp1 across multiple mouse and human datasets.
endogenous growth hormone induces UCP1 expression in adipose tissue via STAT5
Pyruvate induces torpor in obese mice. Pyruvate does not induce torpor in lean mice but results in the activation of brown adipose tissue with an increase in the level of uncoupling protein-1.
striking reduction of mitochondrial electron transport chain components in mice genetically lacking UCP1
UCP1 cannot be fully inhibited by all adenine nucleotides tested. Phosphate is a novel inhibitor of UCP3 and UCP1. Conserved arginines in the PN-binding pocket are involved in the inhibition of UCP1 and UCP3 to different extents. Fatty acids compete with all PNs bound to UCP1.
UCP1 mRNA expression is increased significantly with 10 muM of ACTH.
Data suggest that triiodothyronine and high glucose signal coordinately to up-regulate ChREBP, Ucp1, Glut4, and Fasn in brown adipocytes; ChREBP plays role as a central regulator of brown adipocyte activity/energy metabolism. (ChREBP = carbohydrate-responsive element-binding protein; Ucp1 = uncoupling protein-1; Glut4 = facilitated glucose transporter-4; Fasn = fatty acid synthase, type-I)
expressed in tail sebaceous glands; data do not support a thermoregulatory role
UCP1 expression under inflammation is mediated by the increased expression of DBC1, which inhibits SIRT1 activity.
The results of the present study provide an insight into the unexpected expression of Ucp1 in bovine skeletal muscle, which suggests the necessity for further studies on Ucp1-mediated energy expenditure in bovine skeletal muscle.
study suggests that uncoupling protein 1 affects milk yield, milk fat percentage and milk protein percentage
UCPs do have uncoupling properties when expressed in mitochondria but that uncoupling by UCP1 or UCP2 does not prevent acute substrate-driven endothelial cell superoxide as effluxed from mitochondria respiring in vitro.
These results suggest that CIDE-A and UCP1 are regulated by insulin and/or fatty acids in mammary epithelial cells and lactating mammary glands, and thereby play an important role in lipid and energy metabolism.
Mitochondrial uncoupling proteins (UCP) are members of the family of mitochondrial anion carrier proteins (MACP). UCPs separate oxidative phosphorylation from ATP synthesis with energy dissipated as heat, also referred to as the mitochondrial proton leak. UCPs facilitate the transfer of anions from the inner to the outer mitochondrial membrane and the return transfer of protons from the outer to the inner mitochondrial membrane. They also reduce the mitochondrial membrane potential in mammalian cells. Tissue specificity occurs for the different UCPs and the exact methods of how UCPs transfer H+/OH- are not known. UCPs contain the three homologous protein domains of MACPs. This gene is expressed only in brown adipose tissue, a specialized tissue which functions to produce heat.
uncoupling protein 1 (mitochondrial, proton carrier)
, uncoupling protein 1
, mitochondrial brown fat uncoupling protein 1
, solute carrier family 25 member 7
, UCP 1
, uncoupling protein 1 UCP1
, uncoupling protein 1, mitochondrial
, uncoupling protein, mitochondrial
, mitochondrial, proton carrier
, Solute carrier family 25 member 7