ADP-Glucose (sodium salt)
(Synonyms: 5'-二磷酸葡萄糖腺苷二钠盐,Adenosine-5'-diphosphoglucose, ? ADPG) 目录号 : GC42736An intermediate in polysaccharide synthesis
Cas No.:102129-65-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
ADP-Glucose (ADPG) is an immediate precursor used in the biosynthesis, by glucose addition, of storage polysaccharides in plants, green algae, and cyanobacteria, as well as structural polysaccharides in certain bacteria.[1],[2] It is used by amylose synthases or starch synthases in plastids in the production of amylose, amylopectins, starch, and other polysaccharides. ADPG is normally generated within plastids, although it can be biosynthesized in the cytoplasm of certain grasses and imported into plastids by a membrane-bound transporter.[3]
Reference:
[1]. Ball, S.G., and Morell, M.K. From bacterial glycogen to starch: understanding the biogenesis of the plant starch granule. Annu.Rev.Plant Biol. 54, 207-233 (2003).
[2]. Sambou, T., Dinadayala, P., Stadthagen, G., et al. Capsular glucan and intracellular glycogen of Mycobacterium tuberculosis: Biosynthesis and impact on the presistence in mice. Molecular Microbiology 70(3), 762-774 (2008).
[3]. Comparot-Moss, S., and Denyer, K. The evolution of the startch biosynthetic pathway in cereals and other grasses. Journal of Experimental Botany 60(9), 2481-2492 (2009).
| Cas No. | 102129-65-7 | SDF | |
| 别名 | 5'-二磷酸葡萄糖腺苷二钠盐,Adenosine-5'-diphosphoglucose, ? ADPG | ||
| 化学名 | adenosine 5'-(trihydrogen diphosphate), P'-β-D-glucopyranosyl ester, disodium salt | ||
| Canonical SMILES | O[C@H]1[C@H](N2C=NC3=C2N=CN=C3N)O[C@H](COP(OP(O[C@H]4[C@H](O)[C@@H](O)[C@H](O)[C@@H](CO)O4)([O-])=O)([O-])=O)[C@H]1O.[Na+].[Na+] | ||
| 分子式 | C16H23N5O15P2•2Na | 分子量 | 633.3 |
| 溶解度 | 10mg/mL in PBS, pH7.2 | 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 | 1.579 mL | 7.8952 mL | 15.7903 mL |
| 5 mM | 0.3158 mL | 1.579 mL | 3.1581 mL |
| 10 mM | 0.1579 mL | 0.7895 mL | 1.579 mL |
| 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 | 只 |
| 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 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Lethality caused by ADP-Glucose accumulation is suppressed by salt-induced carbon flux redirection in cyanobacteria
J Exp Bot 2020 Mar 25;71(6):2005-2017.PMID:31858138DOI:10.1093/jxb/erz559.
Cyanobacteria are widely distributed photosynthetic organisms. During the day they store carbon, mainly as glycogen, to provide the energy and carbon source they require for maintenance during the night. Here, we generate a mutant strain of the freshwater cyanobacterium Synechocystis sp. PCC 6803 lacking both glycogen synthases. This mutant has a lethal phenotype due to massive accumulation of ADP-Glucose, the substrate of glycogen synthases. This accumulation leads to alterations in its photosynthetic capacity and a dramatic decrease in the adenylate energy charge of the cell to values as low as 0.1. Lack of ADP-Glucose pyrophosphorylase, the enzyme responsible for ADP-Glucose synthesis, or reintroduction of any of the glycogen synthases abolishes the lethal phenotype. Viability of the glycogen synthase mutant is also fully recovered in NaCl-supplemented medium, which redirects the surplus of ADP-Glucose to synthesize the osmolite glucosylglycerol. This alternative metabolic sink also suppresses phenotypes associated with the defective response to nitrogen deprivation characteristic of glycogen-less mutants, restoring the capacity to degrade phycobiliproteins. Thus, our system is an excellent example of how inadequate management of the adenine nucleotide pools results in a lethal phenotype, and the influence of metabolic carbon flux in cell viability and fitness.
Glycogen formation in Corynebacterium glutamicum and role of ADP-Glucose pyrophosphorylase
Microbiology (Reading) 2007 Apr;153(Pt 4):1275-1285.PMID:17379737DOI:10.1099/mic.0.2006/003368-0.
Glycogen is generally assumed to serve as a major reserve polysaccharide in bacteria. In this work, glycogen accumulation in the amino acid producer Corynebacterium glutamicum was characterized, expression of the C. glutamicum glgC gene, encoding the key enzyme in glycogen synthesis, ADP-Glucose (ADP-Glc) pyrophosphorylase, was analysed, and the relevance of this enzyme for growth, survival, amino acid production and osmoprotection was investigated. C. glutamicum cells grown in medium containing the glycolytic substrates glucose, sucrose or fructose showed rapid glycogen accumulation (up to 90 mg per g dry weight) in the early exponential growth phase and degradation of the polymer when the sugar became limiting. In contrast, no glycogen was detected in cells grown on the gluconeogenic substrates acetate or lactate. In accordance with these results, the specific activity of ADP-Glc pyrophosphorylase was 20-fold higher in glucose-grown than in acetate- or lactate-grown cells. Expression analysis suggested that this carbon-source-dependent regulation might be only partly due to transcriptional control of the glgC gene. Inactivation of the chromosomal glgC gene led to the absence of ADP-Glc pyrophosphorylase activity, to a complete loss of intracellular glycogen in all media tested and to a distinct lag phase when the cells were inoculated in minimal medium containing 750 mM sodium chloride. However, the growth of C. glutamicum, its survival in the stationary phase and its glutamate and lysine production were not affected by glgC inactivation under either condition tested. These results indicate that intracellular glycogen formation is not essential for growth and survival of and amino acid production by C. glutamicum and that ADP-Glc pyrophosphorylase activity might be advantageous for fast adaptation of C. glutamicum to hyperosmotic stress.
Gentisic acid sodium salt, a phenolic compound, is superior to norepinephrine in reversing cardiovascular collapse, hepatic mitochondrial dysfunction and lactic acidemia in Pseudomonas aeruginosa septic shock in dogs
Intensive Care Med Exp 2016 Dec;4(1):24.PMID:27456956DOI:10.1186/s40635-016-0095-0.
Background: The development of lactic acidemia (LA) in septic shock (SS) is associated with an ominous prognosis. We previously showed that the mechanism of LA in SS may relate to impaired hepatic uptake of lactate, but the mechanism was not clear. Uptake of lactate by the liver occurs by a membrane-associated, pH-dependent, antiport system known as the monocarboxylate transporter. In the hepatocyte, lactate can then be metabolized by oxidative phosphorylation or converted to glucose in the cytosol. In the present study, we examined (1) whether hepatic mitochondrial dysfunction accounted for decreased uptake of lactate in a canine model of Pseudomonas aeruginosa SS, (2) whether norepinephrine (NE) treatment by increasing mean arterial pressure (MAP) could improve mitochondrial dysfunction and LA in this model, and (3) whether gentisic acid sodium salt (GSS), a novel phenolic compound, was superior to NE in these effects. Methods: In anesthetized/ventilated dogs, we infused the bacteria over ~10 h and measured hemodynamics in various treatment groups (see below). We then euthanized the animal and isolated the hepatic mitochondria. We measured hepatic mitochondrial oxygen consumption rates using the novel Seahorse XF24 analyzer under conditions that included: basal respiration, after the addition of adenosine- diphosphate to produce coupled respiration, and after the addition of a protonophore to produce maximal respiration. Results: We found that in the septic control group, mean arterial pressure decreased over the course of the study, and that mitochondrial dysfunction developed in which there was a reduction in maximal respiration. Whereas both NE and GSS treatments reversed the reduction in mean arterial pressure and increased maximal respiration to similar extents in respective groups, only in the GSS group was there a reduction in LA. Conclusions: Hepatic mitochondrial dysfunction occurs in SS, but does not appear to be required for the development of LA in SS, since NE improved mitochondrial dysfunction without reversing LA. GSS, a phenolic compound restored mean arterial pressure, mitochondrial dysfunction, and LA in SS. This reduction in LA may be independent of its effect on improving hepatic mitochondrial function.
Mechanisms underlying reduced P2Y(1) -receptor-mediated relaxation in superior mesenteric arteries from long-term streptozotocin-induced diabetic rats
Acta Physiol (Oxf) 2013 Jan;207(1):130-41.PMID:22759594DOI:10.1111/j.1748-1716.2012.02469.x.
Aim: Extracellular nucleotides activate cell-surface purinergic (P2) receptors, contribute to the local regulation of vascular tone and play important roles in pathophysiological states. However, little is known about the vasodilator effects of P2Y(1) -receptor activation in diabetic states. We hypothesized that in a model of established type 1 diabetes, long-term streptozotocin (STZ)-induced diabetic rats, the arterial relaxation elicited by a P2Y(1) -receptor agonist would be impaired. Methods: Relaxations to adenosine 5'-diphosphate sodium salt (ADP), 2-MeSADP (selective P2Y(1) -receptor agonist) and adenosine 5'-triphosphate disodium salt (ATP) were examined in superior mesenteric artery rings from long-term STZ-induced diabetic rats (at 50-57 weeks after STZ injection). ADP-stimulated nitric oxide (NO) production in the superior mesenteric artery was assessed by measuring the levels of NO metabolites. Mesenteric artery expressions of P2Y(1) receptor, and ADP-stimulated levels of phosphorylated endothelial NO synthase (eNOS) (at Ser(1177) and at Thr(495) ) and eNOS were detected by Western blotting. Results: Arteries from diabetic rats exhibited (vs. those from age-matched control rats): (i) reduced ADP-induced relaxation, which was partly or completely inhibited by endothelial denudation, by NOS inhibitor treatment and by a selective P2Y(1) -receptor antagonist, (ii) reduced 2-MeSADP-induced relaxation, (iii) reduced ADP-stimulated release of NO metabolites and (iv) impaired ADP-induced stimulation of eNOS activity (as evidenced by reduced the fold increase in eNOS phosphorylation at Ser(1177) with no difference in fold increase in eNOS phosphorylation at Thr(495) ). The protein expression of P2Y(1) receptor did not differ between diabetic and control arteries. Conclusions: These results suggest that P2Y(1) -receptor-mediated vasodilatation is impaired in superior mesenteric arteries from long-term type 1 diabetic rats. This impairment is because of reduced P2Y(1) -receptor-mediated NO signalling, rather than to reduced P2Y(1) -receptor expression.
Carbohydrate metabolism in mutants of the cyanobacterium Synechococcus elongatus PCC 7942 defective in glycogen synthesis
Appl Environ Microbiol 2010 May;76(10):3153-9.PMID:20363800DOI:10.1128/AEM.00397-08.
ADP-Glucose pyrophosphorylase (AGPase) and glycogen synthase (GS) catalyze the first two reactions of glycogen synthesis in cyanobacteria. Mutants defective in each of these enzymes in Synechococcus elongatus PCC 7942 were constructed and characterized. Activities of the corresponding enzymes in the selected mutants were virtually undetectable, and their ability to synthesize glycogen was entirely abolished. The maximal activities of photosynthetic O(2) evolution and the rates of respiration in the dark were significantly decreased in the mutants compared to those in wild-type cells. Addition of 0.2 M NaCl or 3 mM H(2)O(2) to liquid cultures markedly inhibited the growth of the AGPase and GS mutants, while the same treatment had only marginal effects on the wild type. These results suggest a significant role for storage polysaccharides in tolerance to salt or oxidative stress.