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call loadScript javascripts\jsmol\core\package.js call loadScript javascripts\jsmol\core\core.z.js -- required by ClazzNode call loadScript javascripts\jsmol\J\awtjs2d\WebOutputChannel.js
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Mus musculus
(NCBI:txid10090)
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Source: BioModels - MODEL1507180067
See:
PubMed
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Chlamydomonas reinhardtii
(NCBI:txid3055)
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See:
PubMed
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Escherichia coli
(NCBI:txid562)
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See:
PubMed
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Bronsted base
A molecular entity capable of accepting a hydron from a donor (Bronsted acid).
(via organic amino compound )
Bronsted acid
A molecular entity capable of donating a hydron to an acceptor (Bronsted base).
(via oxoacid )
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Escherichia coli metabolite
Any bacterial metabolite produced during a metabolic reaction in Escherichia coli.
micronutrient
Any nutrient required in small quantities by organisms throughout their life in order to orchestrate a range of physiological functions.
mouse metabolite
Any mammalian metabolite produced during a metabolic reaction in a mouse (Mus musculus).
ferroptosis inducer
Any substance that induces or promotes ferroptosis (a type of programmed cell death dependent on iron and characterized by the accumulation of lipid peroxides) in organisms.
neurotransmitter
An endogenous compound that is used to transmit information across the synapse between a neuron and another cell.
fundamental metabolite
Any metabolite produced by all living cells.
(via glutamic acid )
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nutraceutical
A product in capsule, tablet or liquid form that provide essential nutrients, such as a vitamin, an essential mineral, a protein, an herb, or similar nutritional substance.
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View more via ChEBI Ontology
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(2S)-2-aminopentanedioic acid
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L-glutamic acid
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acide glutamique
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ChEBI
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ácido glutámico
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ChEBI
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acidum glutamicum
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ChEBI
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glutamic acid
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ChEBI
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(S)-2-aminopentanedioic acid
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ChEBI
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(S)-glutamic acid
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NIST Chemistry WebBook
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E
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ChEBI
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Glu
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ChEBI
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Glutamate
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KEGG COMPOUND
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GLUTAMIC ACID
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PDBeChem
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L-Glu
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ChEBI
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L-Glutamic acid
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KEGG COMPOUND
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L-Glutaminic acid
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KEGG COMPOUND
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L-Glutaminsäure
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ChEBI
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1310
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DrugCentral
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2297
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BPDB
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C00001358
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KNApSAcK
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C00025
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KEGG COMPOUND
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D00007
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KEGG DRUG
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DB00142
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DrugBank
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GLT
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MetaCyc
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GLU_LFOH
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PDBeChem
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HMDB0000148
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HMDB
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L-Glutamic_Acid
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Wikipedia
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LSM-36375
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LINCS
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| View more database links |
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1723801
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Reaxys Registry Number
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Reaxys
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3502
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Gmelin Registry Number
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Gmelin
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56-86-0
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CAS Registry Number
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KEGG COMPOUND
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56-86-0
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CAS Registry Number
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ChemIDplus
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56-86-0
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CAS Registry Number
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NIST Chemistry WebBook
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Bordbar A, Mo ML, Nakayasu ES, Schrimpe-Rutledge AC, Kim YM, Metz TO, Jones MB, Frank BC, Smith RD, Peterson SN, Hyduke DR, Adkins JN, Palsson BO (2012)
Model-driven multi-omic data analysis elucidates metabolic immunomodulators of macrophage activation.
Molecular systems biology 8, 558 [PubMed:22735334]
[show Abstract]
Macrophages are central players in immune response, manifesting divergent phenotypes to control inflammation and innate immunity through release of cytokines and other signaling factors. Recently, the focus on metabolism has been reemphasized as critical signaling and regulatory pathways of human pathophysiology, ranging from cancer to aging, often converge on metabolic responses. Here, we used genome-scale modeling and multi-omics (transcriptomics, proteomics, and metabolomics) analysis to assess metabolic features that are critical for macrophage activation. We constructed a genome-scale metabolic network for the RAW 264.7 cell line to determine metabolic modulators of activation. Metabolites well-known to be associated with immunoactivation (glucose and arginine) and immunosuppression (tryptophan and vitamin D3) were among the most critical effectors. Intracellular metabolic mechanisms were assessed, identifying a suppressive role for de-novo nucleotide synthesis. Finally, underlying metabolic mechanisms of macrophage activation are identified by analyzing multi-omic data obtained from LPS-stimulated RAW cells in the context of our flux-based predictions. Our study demonstrates metabolism's role in regulating activation may be greater than previously anticipated and elucidates underlying connections between activation and metabolic effectors. | Aizawa S, Sakai T, Sakata I (2012)
Glutamine and glutamic acid enhance thyroid-stimulating hormone β subunit mRNA expression in the rat pars tuberalis.
The Journal of endocrinology 212, 383-394 [PubMed:22219301]
[show Abstract]
Thyroid-stimulating hormone (TSH)-producing cells of the pars tuberalis (PT) display distinct characteristics that differ from those of the pars distalis (PD). The mRNA expression of TSHβ and αGSU in PT has a circadian rhythm and is inhibited by melatonin via melatonin receptor type 1; however, the detailed regulatory mechanism for TSHβ expression in the PT remains unclear. To identify the factors that affect PT, a microarray analysis was performed on laser-captured PT tissue to screen for genes coding for receptors that are abundantly expressed in the PT. In the PT, we found high expression of the KA2, which is an ionotropic glutamic acid receptor (iGluR). In addition, the amino acid transporter A2 (ATA2), also known as the glutamine transporter, and glutaminase (GLS), as well as GLS2, were highly expressed in the PT compared to the PD. We examined the effects of glutamine and glutamic acid on TSHβ expression and αGSU expression in PT slice cultures. l-Glutamine and l-glutamic acid significantly stimulated TSHβ expression in PT slices after 2- and 4-h treatments, and the effect of l-glutamic acid was stronger than that of l-glutamine. In contrast, treatment with glutamine and glutamic acid did not affect αGSU expression in the PT or the expression of TSHβ or αGSU in the PD. These results strongly suggest that glutamine is taken up by PT cells through ATA2 and that glutamic acid locally converted from glutamine by Gls induces TSHβ expression via the KA2 in an autocrine and/or paracrine manner in the PT. | Stamler J, Brown IJ, Daviglus ML, Chan Q, Kesteloot H, Ueshima H, Zhao L, Elliott P, INTERMAP Research Group (2009)
Glutamic acid, the main dietary amino acid, and blood pressure: the INTERMAP Study (International Collaborative Study of Macronutrients, Micronutrients and Blood Pressure).
Circulation 120, 221-228 [PubMed:19581495]
[show Abstract]
BackgroundData are available that indicate an independent inverse relationship of dietary vegetable protein to the blood pressure (BP) of individuals. Here, we assess whether BP is associated with glutamic acid intake (the predominant dietary amino acid, especially in vegetable protein) and with each of 4 other amino acids that are relatively higher in vegetable than animal protein (proline, phenylalanine, serine, and cystine).Methods and resultsThis was a cross-sectional epidemiological study with 4680 persons 40 to 59 years of age from 17 random population samples in China, Japan, the United Kingdom, and the United States. BP was measured 8 times at 4 visits; dietary data (83 nutrients, 18 amino acids) were obtained from 4 standardized, multipass, 24-hour dietary recalls and 2 timed 24-hour urine collections. Dietary glutamic acid (percentage of total protein intake) was inversely related to BP. Across multivariate regression models (model 1, which controlled for age, gender, and sample, through model 5, which controlled for 16 possible nonnutrient and nutrient confounders), estimated average BP differences associated with a glutamic acid intake that was higher by 4.72% of total dietary protein (2 SD) were -1.5 to -3.0 mm Hg systolic and -1.0 to -1.6 mm Hg diastolic (z scores -2.15 to -5.11). Results were similar for the glutamic acid-BP relationship with each of the other amino acids also in the model; eg, with control for 15 variables plus proline, systolic/diastolic pressure differences were -2.7/-2.0 mm Hg (z scores -2.51, -2.82). In these 2-amino acid models, higher intake (by 2 SD) of each of the other amino acids was associated with small BP differences and z scores.ConclusionsDietary glutamic acid may have independent BP-lowering effects, which may contribute to the inverse relation of vegetable protein to BP. | Catarzi D, Colotta V, Varano F (2007)
Competitive AMPA receptor antagonists.
Medicinal research reviews 27, 239-278 [PubMed:16892196]
[show Abstract]
Glutamic acid (Glu) is the major excitatory neurotransmitter in the mammalian central nervous system (CNS) where it is involved in the physiological regulation of different processes. It has been well established that excessive endogenous Glu is associated with many acute and chronic neurodegenerative disorders such as cerebral ischaemia, epilepsy, amiotrophic lateral sclerosis, Parkinson's, and Alzheimer's disease. These data have consequently added great impetus to the research in this field. In fact, many Glu receptor antagonists acting at the N-methyl-D-aspartic acid (NMDA), 2-amino-3-(3-hydroxy-5-methylisoxazol-4-yl)propionic acid (AMPA), and/or kainic acid (KA) receptors have been developed as research tools and potential therapeutic agents. Ligands showing competitive antagonistic action at the AMPA type of Glu receptors were first reported in 1988, and the systemically active 2,3-dihydroxy-6-nitro-7-sulphamoyl-benzo[f]quinoxaline (NBQX) was first shown to have useful therapeutic effects in animal models of neurological disease in 1990. Since then, the quinoxaline template has represented the backbone of various competitive AMPA receptor antagonists belonging to different classes which had been developed in order to increase potency, selectivity and water solubility, but also to prolong the "in vivo" action. Compounds that present better pharmacokinetic properties and less serious adverse effects with respect to the others previously developed are undergoing clinical evaluation. In the near future, the most important clinical application for the AMPA receptor antagonists will probably be as neuroprotectant in neurodegenerative diseases, such as epilepsy, for the treatment of patients not responding to current therapies. The present review reports the history of competitive AMPA receptor antagonists from 1988 up to today, providing a systematic coverage of both the open and patent literature. | Catarzi D, Colotta V, Varano F (2006)
Competitive Gly/NMDA receptor antagonists.
Current topics in medicinal chemistry 6, 809-821 [PubMed:16719819]
[show Abstract]
Glutamic acid (Glu) is the major excitatory neurotransmitter in the mammalian central nervous system (CNS) where it is involved in the physiological regulation of different processes. It has been well established that excessive endogenous Glu is associated with many acute and chronic neurodegenerative disorders such as cerebral ischemia, epilepsy, amiotrophic lateral sclerosis (ALS), Parkinson's and Alzheimer's diseases. In addition to the classical competitive glutamate receptor (GluR) antagonists, much effort has been directed toward the development of many different non-competitive antagonists of these receptors and, among them, compounds blocking the glycine site on the NMDA receptor complex (Gly/NMDA) have been widely investigated. Many Gly/NMDA receptor antagonists showed to be potential therapeutic agents in many neurological diseases such as stroke, epilepsy and neuropathic pain. Some of them, endowed also with favourable physicochemical properties and low secondary undesiderable effects, reached clinical trials. | Yudkoff M, Daikhin Y, Nissim I, Horyn O, Luhovyy B, Luhovyy B, Lazarow A, Nissim I (2005)
Brain amino acid requirements and toxicity: the example of leucine.
The Journal of nutrition 135, 1531S-8S [PubMed:15930465]
[show Abstract]
Glutamic acid is an important excitatory neurotransmitter of the brain. Two key goals of brain amino acid handling are to maintain a very low intrasynaptic concentration of glutamic acid and also to provide the system with precursors from which to synthesize glutamate. The intrasynaptic glutamate level must be kept low to maximize the signal-to-noise ratio upon the release of glutamate from nerve terminals and to minimize the risk of excitotoxicity consequent to excessive glutamatergic stimulation of susceptible neurons. The brain must also provide neurons with a constant supply of glutamate, which both neurons and glia robustly oxidize. The branched-chain amino acids (BCAAs), particularly leucine, play an important role in this regard. Leucine enters the brain from the blood more rapidly than any other amino acid. Astrocytes, which are in close approximation to brain capillaries, probably are the initial site of metabolism of leucine. A mitochondrial branched-chain aminotransferase is very active in these cells. Indeed, from 30 to 50% of all alpha-amino groups of brain glutamate and glutamine are derived from leucine alone. Astrocytes release the cognate ketoacid [alpha-ketoisocaproate (KIC)] to neurons, which have a cytosolic branched-chain aminotransferase that reaminates the KIC to leucine, in the process consuming glutamate and providing a mechanism for the "buffering" of glutamate if concentrations become excessive. In maple syrup urine disease, or a congenital deficiency of branched-chain ketoacid dehydrogenase, the brain concentration of KIC and other branched-chain ketoacids can increase 10- to 20-fold. This leads to a depletion of glutamate and a consequent reduction in the concentration of brain glutamine, aspartate, alanine, and other amino acids. The result is a compromise of energy metabolism because of a failure of the malate-aspartate shuttle and a diminished rate of protein synthesis. | Chen X, Li D, Lü J, Fang F (1997)
[Determination of gamma-aminobutyric acid and glutamic acid in human cerebrospinal fluid by high performance liquid chromatography].
Se pu = Chinese journal of chromatography 15, 237-239 [PubMed:15739367]
[show Abstract]
Gamma-aminobutyric acid (Gaba) and glutamic acid (Glu) are believed to be the major neurotransmitter. Levels in cerebrospinal fluid (CSF) may reflect their metabolism in various neurotic and psychiatric diseases. Measurements of Gaba and Glu in body fluids will help to elucidate their metabolic role and diagnostic value. In the present work, the concentrations of glutamic acid and gamma-aminobutyric acid in human cerebrospinal fluid were determined by reversed-phase high performance liquid chromatography using pre-column derivatized with dansyl chloride and UV detection at 254 nm. The mobile phase was A:CH3OH and B: THF/CH3OH/0.05 mol/L NaAc (pH 6.2) (5/75/420, V/V) with gradient elution. The flow rate was 1 mL/min. CSF samples were deproteinizated with methanol. After centrifugation at 15000 r/min for 10 min, the supernatant was introduced into a screw-capped vial and evaporated to near dryness at 80 degrees C. Derivatization was carried out by the addition of 250 microL of bicarbonate solution (pH 9.8) and 250 microL of dansyl chloride solution (4 g/L) followed by heating at 40 degrees C water bath for 30 min. Extraction was performed with 300 microL of ethyl acetate and the organic layer separated was dried at room temperature under nitrogen. The dry residue was dissolved and injected into the HPLC system. The linear range of the method was 5-1000 micromol/L (r = 0.9988) for Glu and 1-600 micromol/L (r = 0.9984) for Gaba. The lower limit of detection were 0.002 micromol/L and 0.001 micromol/L respectively. The recoveries were 96.9%-98.8% and 97.5%-98.8% and the coefficients of variation of peak height measurements were 2.2%-3.4% and 3.8%-5.6% respectivery. The method enables a simple, rapid and reproducible quantification of Glu and Gaba neurotransmitter. |
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