Home>>Guanosine 5'-monophosphate (sodium salt)

Guanosine 5'-monophosphate (sodium salt) Sale

(Synonyms: GMP, 5'-Guanylic Acid, NSC 20265) 目录号 : GC43797

Guanosine 5'-monophosphate is a nucleotide used in the synthesis of RNA.

Guanosine 5'-monophosphate (sodium salt) Chemical Structure

Cas No.:5550-12-9

规格 价格 库存 购买数量
5g
¥545.00
现货
10g
¥825.00
现货
25g
¥1,230.00
现货
100g
¥3,815.00
现货

电话:400-920-5774 Email: sales@glpbio.cn

Customer Reviews

Based on customer reviews.

Sample solution is provided at 25 µL, 10mM.

产品文档

Quality Control & SDS

View current batch:

产品描述

Guanosine 5'-monophosphate is a nucleotide used in the synthesis of RNA. Upon phosphorylation to GTP, it becomes incorporated into RNA by various RNA polymerases. It can be used to study modulation of glutamatergic neurotransmission.

Chemical Properties

Cas No. 5550-12-9 SDF
别名 GMP, 5'-Guanylic Acid, NSC 20265
Canonical SMILES O[C@H]1[C@@H](O)[C@H](N2C=NC3=C2N=C(N)NC3=O)O[C@@H]1COP([O-])([O-])=O.[Na+].[Na+]
分子式 C10H12N5O8P•2Na 分子量 407.2
溶解度 PBS (pH 7.2): 10 mg/ml 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。
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。

溶解性数据

制备储备液
1 mg 5 mg 10 mg
1 mM 2.4558 mL 12.279 mL 24.558 mL
5 mM 0.4912 mL 2.4558 mL 4.9116 mL
10 mM 0.2456 mL 1.2279 mL 2.4558 mL
  • 摩尔浓度计算器

  • 稀释计算器

  • 分子量计算器

质量
=
浓度
x
体积
x
分子量
 
 
 
*在配置溶液时,请务必参考产品标签上、MSDS / COA(可在Glpbio的产品页面获得)批次特异的分子量使用本工具。

计算

动物体内配方计算器 (澄清溶液)

第一步:请输入基本实验信息(考虑到实验过程中的损耗,建议多配一只动物的药量)
给药剂量 mg/kg 动物平均体重 g 每只动物给药体积 ul 动物数量
第二步:请输入动物体内配方组成(配方适用于不溶于水的药物;不同批次药物配方比例不同,请联系GLPBIO为您提供正确的澄清溶液配方)
% DMSO % % Tween 80 % saline
计算重置

Research Update

Sodium Ferulate Inhibits Rat Cardiomyocyte Hypertrophy Induced by Angiotensin II Through Enhancement of Endothelial Nitric Oxide Synthase/Nitric Oxide/Cyclic Guanosine Monophosphate Signaling Pathway

J Cardiovasc Pharmacol 2022 Aug 1;80(2):251-260.PMID:35416804DOI:10.1097/FJC.0000000000001277.

Sodium ferulate (SF) is the sodium salt of ferulic acid, which is one of the effective components of Angelica sinensis and Lignsticum chuanxiong , and plays an important role in protecting the cardiovascular system. In this study, myocardial hypertrophy was induced by angiotensin II 0.1 μmol/L in neonatal Sprague-Dawley rat ventricular myocytes. Nine groups were designed, that is, normal, normal administration, model, L-arginine (L-arg 1000 μmol/L), SF (50, 100, 200 μmol/L) group, and N G -nitro-L-arg-methyl ester 1500 μmol/L combined with SF 200 μmol/L or L-arg 1000 μmol/L group, respectively. Cardiomyocyte hypertrophy was confirmed by observing histological changes and measurements of cell diameter, protein content and atrial natriuretic factor, and β-myosin heavy chain levels of the cells. Notably, SF could inhibit significantly myocardial hypertrophy of neonatal rat cardiomyocytes in a concentration-dependent manner without producing cytotoxicity, and the levels of nitric oxide, NO synthase (NOS), endothelial NOS, and cyclic guanosine monophosphate were increased, but the level of cyclic adenosine monophosphate was decreased in cardiomyocytes. Simultaneously, levels of protein kinase C beta, Raf-1, and extracellular regulated protein kinase 1/2 (ERK1/2) were downregulated, whereas levels of mitogen-activated protein kinase phosphatase-1 were significantly upregulated. All the beneficial effects of SF were blunted by N G -nitro-L-arg-methyl ester. Overall, these findings reveal that SF can inhibit angiotensin II-induced myocardial hypertrophy of neonatal rat cardiomyocytes, which is closely related to activation of endothelial NOS/NO/cyclic guanosine monophosphate, and inhibition of protein kinase C and mitogen-activated protein kinase signaling pathways.

Self-organization of Guanosine 5'-monophosphate on mica

Colloids Surf B Biointerfaces 2007 Oct 1;59(2):120-7.PMID:17566718DOI:10.1016/j.colsurfb.2007.04.022.

Self-assembled aggregates of Guanosine 5'-monophosphate (GMP) on the surface of muscovite mica were investigated by atomic force microscopy (AFM). Aqueous solutions of sodium, potassium and ammonium GMP salts were studied. For solution concentrations c < 0.005 wt% only small islands of deposited material are present on the surface. For c approximately 0.02 wt%, in addition to the islands and patches, also linear aggregates called G-wires are formed. The wire-like aggregates are on average 1.9 nm high and can be several micrometers long. They exhibit a profound directional growth along the six main crystallographic axes of the basal plane of mica. For c > 0.1 wt% flat terraces with the height of 2.5 nm appear. They are formed of G-wires lying with their long axis parallel to the substrate and stacking in a hexagonal arrangement. The morphology of the adsorbates is independent of the type of salt used to prepare the initial solution. This signifies that intrinsic potassium ions from the substrate play much more important role in the GMP adsorption than cations from the solution.

Sensory and receptor responses to umami: an overview of pioneering work

Am J Clin Nutr 2009 Sep;90(3):723S-727S.PMID:19571221DOI:10.3945/ajcn.2009.27462E.

This article provides a selective overview of the early studies of umami taste and outlines significant questions for further research. Umami compounds such as the amino acid glutamate [often in the form of the sodium salt monosodium glutamate (MSG)] and the nucleotide monophosphates 5'-inosinate and 5'-guanylate occur naturally in, and provide flavor for, many foods and cuisines around the world. Early researchers in the United States found that the flavor of pure MSG was difficult to describe. But they all agreed that, although humans found umami compounds, when tasted alone, to be unpalatable, subjects reported that these compounds improved the taste of foods. This taste "dichotomy" may be partly unlearned because it is also observed in very young infants. The uniqueness of umami perception is based on several lines of evidence. First, numerous perceptual studies have shown that the sensation aroused by MSG is distinct from that of the other 4 taste qualities. Second, biochemical studies that show the synergy of the binding of MSG and 5'-guanylate to tongue taste tissue mirror this hallmark perceptual effect. Third, several specific receptors that may mediate umami taste have recently been identified. There remain, however, a number of puzzles surrounding the umami concept, including the molecular basis for an apparent tactile component to umami perception, the reason for the unpalatability of pure umami, and the functional significance for human health and nutrition of umami detection. Future work aimed at understanding these and other open issues will profitably engage scientists in umami research well into the next century.

Cyclic guanosine monophosphate and the dependent protein kinase regulate lymphatic contractility in rat thoracic duct

J Physiol 2013 Sep 15;591(18):4549-65.PMID:23836689DOI:10.1113/jphysiol.2013.258681.

We have previously demonstrated a principal role for nitric oxide (NO) in the endothelium/shear-dependent regulation of contractility in rat thoracic duct (TD). In this study we tested the hypothesis that cyclic guanosine monophosphate (cGMP) and the dependent protein kinase (PKG) are central to the intrinsic and extrinsic flow-dependent modulation of lymphatic contractility. Lymphatic diameters and indices of pumping in isolated, cannulated and pressurized segments of rat TD were measured. The influences of increased transmural pressure (1-5 cmH2O) and imposed flow (1-5 cm H2O transaxial pressure gradients) on lymphatic function were studied before and after: (1) inhibition of guanylate cyclase (GC) with and without a NO donor; (2) application of stable cGMP analogue; and (3) inhibition of the cGMP activation of PKG. Additionally, Western blotting and immunofluorescent tissue staining were used to analyse the PKG isoforms expressed in TD. We found that the GC inhibitor ODQ induced changes in TD contractility similar to NO synthase blockade and prevented the relaxation induced by the NO donor S-nitroso-N-acetylpenicillamine. The cGMP analogue, 8-(4-Chlorophenylthio)-guanosine 3,5-cyclic monophosphate sodium salt (8pCPTcGMP), mimicked the extrinsic flow-induced relaxation in a dose-dependent manner, whereas treatment with the cGMP/PKG inhibitor, guanosine 3,5-cyclic monophosphorothioate, 8-(4-chlorophenylthio)-, Rp-isomer, triethylammonium salt (Rp-8-Br-PETcGMPS), eliminated intrinsic flow-dependent relaxation, and largely inhibited extrinsic flow-dependent relaxation. Western blotting demonstrated that both PKG-Iα and -Iβ isoforms are found in TD, with ∼10 times greater expression of the PKG-Iα protein in TD compared with the aorta and vena cava. The PKG-Iβ isoform expressed equally in TD and vena cava, both being ∼2 times higher than that in the aorta. Immunofluorescent labelling of PKG-Iα protein in the wall of rat thoracic duct confirmed its localization inside TD muscle cells. These findings demonstrate that cGMP is critical to the flow-dependent regulation of TD contractility; they also indicate an important involvement of PKG, especially PKG-Iα in these processes and identifies PKG protein as a potential therapeutic target.

Linolenic Acid Attenuates the Vasodilation Induced by Acetylcholine in Isolated Rat Aortae

Dose Response 2019 Dec 9;17(4):1559325819894148.PMID:31839761DOI:10.1177/1559325819894148.

This study aims to examine the effect of linolenic acid on the vasodilation or vasoconstriction induced by acetylcholine and bupivacaine in isolated rat aortae and its underlying mechanism. The effect of linolenic acid on the vasodilation induced by acetylcholine, the calcium ionophore A23187, sodium nitroprusside, and 8-bromoguanosine 3',5'-cyclic monophosphate sodium salt (bromo-cyclic guanosine monophosphate [bromo-cGMP]) in endothelium-intact and endothelium-denuded aortae was examined. Linolenic acid inhibited vasodilation induced by acetylcholine, calcium ionophore A23187, and sodium nitroprusside. However, this fatty acid increased bromo-cGMP-induced vasodilation in endothelium-denuded aortae. Linolenic acid increased bupivacaine-induced contraction in endothelium-intact aortae, whereas it decreased bupivacaine-induced contraction in endothelium-intact aortae with Nω-nitro-l-arginine methyl ester and endothelium-denuded aortae. Linolenic acid inhibited acetylcholine- and bupivacaine-induced phosphorylation of endothelial nitric oxide synthase. Sodium nitroprusside increased cGMP in endothelium-denuded aortic strips, whereas bupivacaine decreased cGMP in endothelium-intact aortic strips. Linolenic acid decreased cGMP levels produced by bupivacaine and sodium nitroprusside. Together, these results suggest that linolenic acid inhibits acetylcholine-induced relaxation by inhibiting a step just prior to nitric oxide-induced cGMP formation. In addition, linolenic acid-mediated inhibition of vasodilation induced by a toxic concentration (3 × 10-4 M) of bupivacaine seems to be partially associated with inhibition of the nitric oxide-cGMP pathway.