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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.
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 (show PRDM16 Proteins) mRNA
Results found a specific fatty acids binding site that is functionally important to the H+ transport activity of UCP1-mediated flux.
MKK6 (show MAP2K6 Proteins) 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 Proteins) 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 Proteins) polymorphism, may increase the risk of obesity with synergistic effects. The ins (show INS Proteins) allele of the UCP2 (show UCP2 Proteins) exon 8 del/ins (show INS Proteins) polymorphism may contribute to low HDL (show HSD11B1 Proteins) 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.
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 (show FNDC5 Proteins) 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 (show GH1 Proteins) induces UCP1 expression in adipose tissue via STAT5 (show STAT5A Proteins)
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 (show POMC Proteins).
Data suggest that triiodothyronine and high glucose signal coordinately to up-regulate ChREBP (show MLXIPL Proteins), Ucp1, Glut4 (show SLC2A4 Proteins), and Fasn (show FASN Proteins) in brown adipocytes; ChREBP (show MLXIPL Proteins) plays role as a central regulator of brown adipocyte activity/energy metabolism. (ChREBP (show MLXIPL Proteins) = carbohydrate-responsive element-binding protein (show MLXIPL Proteins); Ucp1 = uncoupling protein-1; Glut4 (show SLC2A4 Proteins) = facilitated glucose transporter (show SLC2A12 Proteins)-4; Fasn (show FASN Proteins) = fatty acid synthase (show FASN Proteins), type-I)
UCP1 expression under inflammation is mediated by the increased expression of DBC1, which inhibits SIRT1 (show SIRT1 Proteins) 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 (show CSN2 Proteins) percentage
UCPs do have uncoupling properties when expressed in mitochondria but that uncoupling by UCP1 or UCP2 (show UCP2 Proteins) does not prevent acute substrate-driven endothelial cell superoxide as effluxed from mitochondria respiring in vitro.
These results suggest that CIDE-A (show CIDEA Proteins) and UCP1 are regulated by insulin (show INS Proteins) 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