Uridine triphosphate (UTP)
(Synonyms: 三磷酸尿苷; UTP; Uridine 5'-triphosphate) 目录号 : GC33830
三磷酸尿苷 (UTP) (UTP;Uridine 5'-triphosphate) 是一种核苷酸，可在正常和疾病状态下调节胰腺在内分泌和外分泌分泌、增殖、通道、转运体和细胞内信号传导方面的功能。
Cas No.:63-39-8
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >98.00%
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Cell experiment: | Pancreatic duct epithelial cells are treated with (0.1 μM-1 mM) uridine triphosphate. BrdU is added after different time points (12-24 hours). Proliferation is measured using the BrdU incorporation assay in triplicate[2]. |
Animal experiment: | Rats: Four main groups are tested: (1) sham without LAD ligation, (2) LAD ligation, (3) injected with UTP (0.44 µg/kg i.v.) 30 min before MI, (4) UTP injection (4.4 µg/kg i.v.) 24 h prior to MI. Several different concentrations of UTP are tested (0.044–44.4 µg/kg). Left ventricular systolic pressure (LVSP), end-diastolic pressure (LVEDP) and heart rates are monitored before, after UTP treatment and post MI[3]. |
References: [1]. Lamarca A, et al. Uridine 5'-triphosphate promotes in vitro Schwannoma cell migration through matrix metalloproteinase-2 activation. PLoS One. 2014 Jun 6;9(6):e98998. | |
Uridine triphosphate (UTP;Uridine 5'-triphosphate) is a pyrimidine nucleoside triphosphate that participates in glycogen metabolism and synthesis of RNA during transcription.
Uridine triphosphate treatment induces Schwannoma cell migration through activation of P2Y2 receptors and through the increase of extracellular matrix metalloproteinase-2 (MMP-2) activation and expression[1]. Uridine triphosphate-induced proliferation is mediated by protein kinase D, Src-family tyrosine kinase, Ca/calmodulin-dependent protein kinase II, phosphatidylinositol 3-kinase (PI3K), Akt, and phospholipase D. Uridine triphosphate increases phosphorylation of Akt through protein kinase C, Src-family tyrosine kinase, Ca/calmodulin-dependent protein kinase II, and PI3K[2].
Uridine triphosphate reduces mitochondrial calcium levels following hypoxia. Early or late uridine triphosphate preconditioning is effective to reduce infarct size and superior myocardial function[3]. Uridine triphosphate treatment increases the number of monocytes and macrophages infiltrating the pouch and up-regulates the gene expression of IL-4 and IL-13 in the regional lymph nodes[4].
[1]. Lamarca A, et al. Uridine 5'-triphosphate promotes in vitro Schwannoma cell migration through matrix metalloproteinase-2 activation. PLoS One. 2014 Jun 6;9(6):e98998. [2]. Choi JH, et al. Uridine triphosphate increases proliferation of human cancerous pancreatic duct epithelial cells by activating P2Y2 receptor. Pancreas. 2013 May;42(4):680-6. [3]. Yitzhaki S, et al. Uridine-5'-triphosphate (UTP) reduces infarct size and improves rat heart function aftermyocardial infarct. Biochem Pharmacol. 2006 Oct 16;72(8):949-55. [4]. Iwaki Y, et al. Enhancement of antibody production against rabies virus by uridine 5'-triphosphate in mice. Microbes Infect. 2014 Mar;16(3):196-202.
| Cas No. | 63-39-8 | SDF | |
| 别名 | 三磷酸尿苷; UTP; Uridine 5'-triphosphate | ||
| Canonical SMILES | O[C@H]1[C@H](N2C(NC(C=C2)=O)=O)O[C@H](COP(OP(OP(O)(O)=O)(O)=O)(O)=O)[C@H]1O | ||
| 分子式 | C9H15N2O15P3 | 分子量 | 484.14 |
| 溶解度 | Water : ≥ 150 mg/mL (309.83 mM) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.0655 mL | 10.3276 mL | 20.6552 mL |
| 5 mM | 0.4131 mL | 2.0655 mL | 4.131 mL |
| 10 mM | 0.2066 mL | 1.0328 mL | 2.0655 mL |
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动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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Uridine triphosphate (UTP) is released during cardiac ischemia
Int J Cardiol 2005 Apr 28;100(3):427-33.PMID:15837087DOI:10.1016/j.ijcard.2004.10.005.
Background: Extracellular Uridine triphosphate (UTP) stimulates vasodilatation, automaticity in ventricular myocytes and release of tissue-plasminogen activator (t-PA), indicating that UTP may be important in cardiac regulation. We took advantage of a recently developed quantitative assay for UTP to test the hypothesis that UTP is released in the circulation during cardiac ischemia. Methods: In ten pigs, a balloon catheter in the left anterior descending artery was introduced to induce ischemia. Samples were collected from the coronary sinus. Blood flow in the coronary sinus was assessed by a Doppler velocity transducer. Results: Plasma UTP levels increased early during ischemia and early after reperfusion (by 257+/-100 and 247+/-72%, p<0.05). Cardiac blood flow, ventricular arrhythmias and t-PA release were markedly increased at the same time points. In contrast, after 30 min, a second period of ischemia did not result in any significant increase of UTP or blood flow. Furthermore, ventricular arrhythmias were less frequent. UTP levels correlated with ventricular arrhythmia and blood flow. Similar results were found for ATP. Conclusion: For the first time we have shown that UTP is released during cardiac ischemia. UTP released during ischemia may stimulate blood flow, arrhythmia and t-PA release.
Uridine-5'-triphosphate (UTP) maintains cardiac mitochondrial function following chemical and hypoxic stress
J Mol Cell Cardiol 2007 Nov;43(5):653-62.PMID:17880998DOI:10.1016/j.yjmcc.2007.07.060.
Previously we found that uridine-5'-triphosphate (UTP) significantly decreased cultured cardiomyocyte death, induced by hypoxia via activating P2Y(2) receptors, reduced infarct size and maintained higher ATP levels in an in vivo model. Mitochondrial contribution to the progression of cardiomyocyte injury in ischemia/hypoxia is well known. However, the protective effects of UTP in cardiac cells with a respiratory chain deficiency are poorly elucidated. The aim of our study was to further define the role of UTP on mitochondrial functional tolerance following chemical and/or ischemic stress in in vivo and in vitro models. Cardiac mitochondrial function was tested 24 h post left anterior descending (LAD) ligation in UTP (0.44 microg/kg)-treated rats. UTP's beneficial effect in LAD-ligated hearts was expressed by improved mitochondrial activity (Complexes I, II and IV). In the in vitro model, cultured cardiomyocytes were pretreated with 50 microM UTP prior to hypoxic and/or chemical stress with rotenone or sodium azide. Pretreatment with UTP maintained increased ATP levels as well as mitochondrial membrane potential and reduced lactate dehydrogenase (LDH) release. A modest reduction (12%) in the mitochondrial membrane potential was demonstrated when the cultured cardiomyocytes were subjected to UTP. This reduction was abolished by the P2Y receptor antagonist, reactive blue 2, but not with 5 hydroxydecanoate, a mitochondrial K(ATP) channel inhibitor, or by BAPTA-AM, the intracellular calcium chelator. We suggest that UTP may act as an uncoupling agent, which exerts a modest mitochondrial depolarization, resulting in a reduction of Ca(2+) uptake, preserving mitochondrial activity, thereby reducing cell damage during hypoxia.
Uridine Triphosphate Thio Analogues Inhibit Platelet P2Y12 Receptor and Aggregation
Int J Mol Sci 2017 Jan 29;18(2):269.PMID:28146050DOI:10.3390/ijms18020269.
Platelet P2Y12 is an important adenosine diphosphate (ADP) receptor that is involved in agonist-induced platelet aggregation and is a valuable target for the development of anti-platelet drugs. Here we characterise the effects of thio analogues of Uridine triphosphate (UTP) on ADP-induced platelet aggregation. Using human platelet-rich plasma, we demonstrate that UTP inhibits P2Y12 but not P2Y₁ receptors and antagonises 10 µM ADP-induced platelet aggregation in a concentration-dependent manner with an IC50 value of ~250 °µM. An eight-fold higher platelet inhibitory activity was observed with a 2-thio analogue of UTP (2S-UTP), with an IC50 of 30 µM. The 4-thio analogue (4S-UTP) with an IC50 of 7.5 µM was 33-fold more effective. A three-fold decrease in inhibitory activity, however, was observed by introducing an isobutyl group at the 4S- position. A complete loss of inhibition was observed with thio-modification of the γ phosphate of the sugar moiety, which yields an enzymatically stable analogue. The interaction of UTP analogues with P2Y12 receptor was verified by P2Y12 receptor binding and cyclic AMP (cAMP) assays. These novel data demonstrate for the first time that 2- and 4-thio analogues of UTP are potent P2Y12 receptor antagonists that may be useful for therapeutic intervention.
Purinergic signaling in scarring
FASEB J 2016 Jan;30(1):3-12.PMID:26333425DOI:10.1096/fj.15-274563.
Adenosine (ADO) and nucleotides such as ATP, ADP, and uridine 5'-triphosphate (UTP), among others, may serve as extracellular signaling molecules. These mediators activate specific cell-surface receptors-namely, purinergic 1 and 2 (P1 and P2)-to modulate crucial pathophysiological responses. Regulation of this process is maintained by nucleoside and nucleotide transporters, as well as the ectonucleotidases ectonucleoside triphosphate diphosphohydrolase [ENTPD; cluster of differentiation (CD)39] and ecto-5'-nucleotidase (5'-NT; CD73), among others. Cells involved in tissue repair, healing, and scarring respond to both ADO and ATP. Our recent investigations have shown that modulation of purinergic signaling regulates matrix deposition during tissue repair and fibrosis in several organs. Cells release adenine nucleotides into the extracellular space, where these mediators are converted by CD39 and CD73 into ADO, which is anti-inflammatory in the short term but may also promote dermal, heart, liver, and lung fibrosis with repetitive signaling under defined circumstances. Extracellular ATP stimulates cardiac fibroblast proliferation, lung inflammation, and fibrosis. P2Y2 (UTP/ATP) and P2Y6 [ADP/UTP/uridine 5'-diphosphate (UDP)] have been shown to have profibrotic effects, as well. Modulation of purinergic signaling represents a novel approach to preventing or diminishing fibrosis. We provide an overview of the current understanding of purinergic signaling in scarring and discuss its potential to prevent or decrease fibrosis.
Pathway Optimization and Uridine 5'-Triphosphate Regeneration for Enhancing Lacto- N-Tetraose Biosynthesis in Engineered Escherichia coli
J Agric Food Chem 2022 Jun 29;70(25):7727-7735.PMID:35723433DOI:10.1021/acs.jafc.2c02426.
Recently, human milk oligosaccharides (HMOs) have attracted increasing attention and display great commercial importance, especially for the infant formula industry. Lacto-N-tetraose (LNT) is an important neutral HMO commercially added in infant formula and a core structure for synthesizing complex HMOs. Previously, a novel LNT-generating β-1,3-galactosyltransferase from Pseudogulbenkiania ferrooxidans was identified and used for construction of an LNT-producing engineered Escherichia coli. In this work, LNT biosynthesis was further enhanced by pathway optimization and uridine 5'-triphosphate (UTP) regeneration. The main strategies included genomic integration of UDP-glucose 4-epimerase-encoding gene, fine-tuning of the LNT pathway-related genes, blocking of competitive pathways related to UDP-galactose, and overexpression of UTP supply related genes. The maximal LNT titer reached 6.16 and 57.5 g/L by shake-flask and fed-batch fermentation, respectively.