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Glutaric acid Sale

(Synonyms: 戊二酸) 目录号 : GC33814

Glutaric acid (GA) is an attractive C5 dicarboxylic acid with wide applications in the biochemical industry.

Glutaric acid Chemical Structure

Cas No.:110-94-1

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产品描述

Glutaric acid (GA) is an attractive C5 dicarboxylic acid with wide applications in the biochemical industry.

[1] Soo-Yeon Yang, et al. Enzyme Microb Technol. 2019 Sep;128:72-78.

Chemical Properties

Cas No. 110-94-1 SDF
别名 戊二酸
Canonical SMILES O=C(O)CCCC(O)=O
分子式 C5H8O4 分子量 132.12
溶解度 DMSO: 125 mg/mL (946.11 mM) 储存条件 Store at -20°C
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1 mM 7.5689 mL 37.8444 mL 75.6888 mL
5 mM 1.5138 mL 7.5689 mL 15.1378 mL
10 mM 0.7569 mL 3.7844 mL 7.5689 mL
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Research Update

Proposed recommendations for diagnosing and managing individuals with glutaric aciduria type I: second revision

J Inherit Metab Dis 2017 Jan;40(1):75-101.PMID:27853989DOI:10.1007/s10545-016-9999-9.

Glutaric aciduria type I (GA-I; synonym, glutaric acidemia type I) is a rare inherited metabolic disease caused by deficiency of glutaryl-CoA dehydrogenase located in the catabolic pathways of L-lysine, L-hydroxylysine, and L-tryptophan. The enzymatic defect results in elevated concentrations of Glutaric acid, 3-hydroxyglutaric acid, glutaconic acid, and glutaryl carnitine in body tissues, which can be reliably detected by gas chromatography/mass spectrometry (organic acids) and tandem mass spectrometry (acylcarnitines). Most untreated individuals with GA-I experience acute encephalopathic crises during the first 6 years of life that are triggered by infectious diseases, febrile reaction to vaccinations, and surgery. These crises result in striatal injury and consequent dystonic movement disorder; thus, significant mortality and morbidity results. In some patients, neurologic disease may also develop without clinically apparent crises at any age. Neonatal screening for GA-I us being used in a growing number of countries worldwide and is cost effective. Metabolic treatment, consisting of low lysine diet, carnitine supplementation, and intensified emergency treatment during catabolism, is effective treatment and improves neurologic outcome in those individuals diagnosed early; treatment after symptom onset, however, is less effective. Dietary treatment is relaxed after age 6 years and should be supervised by specialized metabolic centers. The major aim of this second revision of proposed recommendations is to re-evaluate the previous recommendations (Kölker et al. J Inherit Metab Dis 30:5-22, 2007b; J Inherit Metab Dis 34:677-694, 2011) and add new research findings, relevant clinical aspects, and the perspective of affected individuals.

Enhancing Glutaric acid production in Escherichia coli by uptake of malonic acid

J Ind Microbiol Biotechnol 2020 Mar;47(3):311-318.PMID:32140931DOI:10.1007/s10295-020-02268-6.

Glutaric acid is an important organic acid applied widely in different fields. Most previous researches have focused on the production of Glutaric acid in various strains using the 5-aminovaleric acid (AMV) or pentenoic acid synthesis pathways. We previously utilized a five-step reversed adipic acid degradation pathway (RADP) in Escherichia coli BL21 (DE3) to construct strain Bgl146. Herein, we found that malonyl-CoA was strictly limited in this strain, and increasing its abundance could improve Glutaric acid production. We, therefore, constructed a malonic acid uptake pathway in E. coli using matB (malonic acid synthetase) and matC (malonic acid carrier protein) from Clover rhizobia. The titer of Glutaric acid was improved by 2.1-fold and 1.45-fold, respectively, reaching 0.56 g/L and 4.35 g/L in shake flask and batch fermentation following addition of malonic acid. Finally, the highest titer of Glutaric acid was 6.3 g/L in fed-batch fermentation at optimized fermentation conditions.

Development of a Glutaric acid production system equipped with stepwise feeding of monosodium glutamate by whole-cell bioconversion

Enzyme Microb Technol 2022 Sep;159:110053.PMID:35537377DOI:10.1016/j.enzmictec.2022.110053.

In the bioproduction of Glutaric acid, an emerging bioplastic monomer, α-ketoglutaric acid (α-KG) is required as an amine acceptor for 4-aminobutyrate aminotransferase (GabT)-driven conversion of 5-aminovalerate (5-AVA) to glutarate semialdehyde. Herein, instead of using expensive α-KG, an indirect α-KG supply system was developed using a relatively cheap alternative, monosodium glutamate (MSG), for l-glutamate oxidase (Gox)-based whole-cell conversion. Using 200 mM 5-AVA and 30 mM MSG initially with Gox, 67.1 mM of Glutaric acid was produced. By applying the stepwise feeding strategy of MSG, the Glutaric acid production capability was increased to 159.1 mM Glutaric acid with a conversion yield of 79.6%. In addition, a buffer-free one-pot reaction from l-lysine was also applied in a 5 L bioreactor to evaluate its industrial applicability, resulting in a conversion yield of 54.2%. The system developed herein might have great potential for the large-scale, economically feasible production of Glutaric acid by whole-cell conversion.

Glutaric acid production by systems metabolic engineering of an l-lysine-overproducing Corynebacterium glutamicum

Proc Natl Acad Sci U S A 2020 Dec 1;117(48):30328-30334.PMID:33199604DOI:10.1073/pnas.2017483117.

There is increasing industrial demand for five-carbon platform chemicals, particularly Glutaric acid, a widely used building block chemical for the synthesis of polyesters and polyamides. Here we report the development of an efficient Glutaric acid microbial producer by systems metabolic engineering of an l-lysine-overproducing Corynebacterium glutamicum BE strain. Based on our previous study, an optimal synthetic metabolic pathway comprising Pseudomonas putida l-lysine monooxygenase (davB) and 5-aminovaleramide amidohydrolase (davA) genes and C. glutamicum 4-aminobutyrate aminotransferase (gabT) and succinate-semialdehyde dehydrogenase (gabD) genes, was introduced into the C. glutamicum BE strain. Through system-wide analyses including genome-scale metabolic simulation, comparative transcriptome analysis, and flux response analysis, 11 target genes to be manipulated were identified and expressed at desired levels to increase the supply of direct precursor l-lysine and reduce precursor loss. A Glutaric acid exporter encoded by ynfM was discovered and overexpressed to further enhance Glutaric acid production. Fermentation conditions, including oxygen transfer rate, batch-phase glucose level, and nutrient feeding strategy, were optimized for the efficient production of Glutaric acid. Fed-batch culture of the final engineered strain produced 105.3 g/L of Glutaric acid in 69 h without any byproduct. The strategies of metabolic engineering and fermentation optimization described here will be useful for developing engineered microorganisms for the high-level bio-based production of other chemicals of interest to industry.

Membrane translocation of Glutaric acid and its derivatives

J Inherit Metab Dis 2008 Apr;31(2):188-93.PMID:18404412DOI:10.1007/s10545-008-0825-x.

The neurodegenerative disorder glutaric aciduria type I (GA I) is characterized by increased levels of cytotoxic metabolites such as Glutaric acid (GA) and 3-hydroxyglutaric (3OHGA). The present report summarizes recent investigations providing insights into mechanisms of intra- and intercellular translocation of these metabolites. Initiated by microarray analyses in a mouse model of GA I, the sodium-dependent dicarboxylate cotransporter 3 (NaC3) was the first molecule identified to mediate the translocation of GA and 3OHGA with high and low affinity, respectively. More recently, organic anion transporters (OAT) 1 and 4 have been reported to be high-affinity transporters for GA and 3OHGA as well as D-2- and L-2-hydroxyglutaric acid (D2OHGA, L2OHGA). The concerted action of NaC3 and OATs may be important for the directed uptake and excretion of GA, 3OHGA, D2OHGA and L2OHGA in kidney proximal tubule cells. In addition, experimental data on cultured neuronal and glial cells isolated from mouse brain demonstrated that GA rather than 3OHGA may competitively inhibit the anaplerotic supply of tricarboxylic acid cycle intermediates from astrocytes to neurons. The identification of GA and GA derivative transporters may represent targets for new approaches to treat patients with GA I and related disorders.