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anti-Human UCP1 Antibodies:
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Human Polyclonal UCP1 Primary Antibody for 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. in Endocrinology 2012
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Human Polyclonal UCP1 Primary Antibody for 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. in The Journal of biological chemistry 2012
Show all 3 Pubmed References
Arabidopsis thaliana Polyclonal UCP1 Primary Antibody for WB - ABIN1720809
Grabelnych, Borovik, Tauson, Pobezhimova, Katyshev, Pavlovskaya, Koroleva, Lyubushkina, Bashmakov, Popov, Borovskii, Voinikov: Mitochondrial energy-dissipating systems (alternative oxidase, uncoupling proteins, and external NADH dehydrogenase) are involved in development of frost-resistance of winter wheat seedlings. in Biochemistry. Biokhimii?a 2014
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]
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.
MKK6 (show MAP2K6 Antibodies) 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 (show UCP2 Antibodies) 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 (show UCP2 Antibodies) polymorphism, may increase the risk of obesity with synergistic effects. The ins (show INS Antibodies) allele of the UCP2 (show UCP2 Antibodies) exon 8 del/ins (show INS Antibodies) polymorphism may contribute to low HDL (show HSD11B1 Antibodies) 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 (show IFNG Antibodies)) or type 2 diabetes mellitus (T2DM) among the residents of Henan province, China. Individuals with the haplotype AAG (show MPG Antibodies) (PPARGC1A gene) and CTCG (UCP1 gene) have increased susceptibility to IFG (show IFNG Antibodies) or T2DM, while those with haplotype AAG (show MPG Antibodies) (PPARGC1A gene) and CTCA (UCP1 gene) have a lower risk of IFG (show IFNG Antibodies) 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 (show BAAT Antibodies) in obese humans. Increased levels of IL6 (show IL6 Antibodies), UCP1 and SIRT1 (show SIRT1 Antibodies) in the BAT (show BAAT Antibodies) were associated with metabolic parameters improvements.
Data suggest that triiodothyronine and high glucose signal coordinately to up-regulate ChREBP (show MLXIPL Antibodies), Ucp1, Glut4 (show SLC2A4 Antibodies), and Fasn (show FASN Antibodies) in brown adipocytes; ChREBP (show MLXIPL Antibodies) plays role as a central regulator of brown adipocyte activity/energy metabolism. (ChREBP (show MLXIPL Antibodies) = carbohydrate-responsive element-binding protein (show MLXIPL Antibodies); Ucp1 = uncoupling protein-1; Glut4 (show SLC2A4 Antibodies) = facilitated glucose transporter (show SLC2A12 Antibodies)-4; Fasn (show FASN Antibodies) = fatty acid synthase (show FASN Antibodies), type-I)
UCP1 expression under inflammation is mediated by the increased expression of DBC1, which inhibits SIRT1 (show SIRT1 Antibodies) activity.
we find that rapamycin inhibits mTORC1 but not mTORC2 (show CRTC2 Antibodies), leading to suppression of elevated lipolysis and restoration of thermogenic protein UCP1 levels, respectively
mTORC1 mediated many of the beneficial actions of FGF21 (show FGF21 Antibodies) in vitro, including UCP1 and FGF21 (show FGF21 Antibodies) induction, increased adiponectin secretion, and enhanced glucose uptake without any adverse effects on insulin (show INS Antibodies) action.
Thus UCP1-dependent diet-induced thermogenesis limits obesity development during exposure to obesogenic diets but does not prevent obesity as such
This study demonstrated that elimination of the gene expressing uncoupling protein-1 (UCP1), the enzyme responsible for thermogenesis, prevented musculoskeletal hyperalgesia in response to either a swim or BRL37344.
Aortic UCP1 content was greater in females than males and its deletion improved ex vivo aortic vasomotor function in females only. Constitutive UCP1 content in BAT (show BAAT Antibodies) was similar between females and males and loss of UCP1 did not abolish sex differences in insulin (show INS Antibodies) sensitivity. Metabolic disruptions caused by UCP1 ablation did not appear to be contingent upon increased oxidative stress in mice under normal dietary conditions.
Gelidium elegans stimulates the expression of PRDM16 (show PRDM16 Antibodies) and UCP-1 Protein in brown adipose tissue and suppresses hyperglycemia in high-fat diet mice.
through interaction with Zfp516 (show ZNF516 Antibodies), LSD1 (show KDM1A Antibodies) is recruited to UCP1 and other brown adipose tissue-enriched genes.
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 (show CSN2 Antibodies) percentage
UCPs do have uncoupling properties when expressed in mitochondria but that uncoupling by UCP1 or UCP2 (show UCP2 Antibodies) does not prevent acute substrate-driven endothelial cell superoxide as effluxed from mitochondria respiring in vitro.
These results suggest that CIDE-A (show CIDEA Antibodies) and UCP1 are regulated by insulin (show INS Antibodies) 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