Phenylacetylglutamine

(2S)-5-amino-5-oxo-2-[(2-phenylacetyl)amino]pentanoic acid

Formula: C13H16N2O4 (264.111)
Chinese Name: N-苯乙酰基-L-谷氨酰胺, 苯乙酰谷氨酰胺
BioDeep ID: BioDeep_00000002938 ( View LC/MS Profile)
SMILES: NC(=O)CC[C@H](NC(=O)CC1=CC=CC=C1)C(O)=O



Found 9 Sample Hits

m/z Adducts Species Organ Scanning Sample
265.1198 [M+H]+
PPM:5.7
Posidonia oceanica root MALDI (CHCA)
20190614_MS1_A19r-20 - MTBLS1746
Resolution: 17μm, 262x276

Description

Seagrasses are one of the most efficient natural sinks of carbon dioxide (CO2) on Earth. Despite covering less than 0.1% of coastal regions, they have the capacity to bury up to 10% of marine organic matter and can bury the same amount of carbon 35 times faster than tropical rainforests. On land, the soil’s ability to sequestrate carbon is intimately linked to microbial metabolism. Despite the growing attention to the link between plant production, microbial communities, and the carbon cycle in terrestrial ecosystems, these processes remain enigmatic in the sea. Here, we show that seagrasses excrete organic sugars, namely in the form of sucrose, into their rhizospheres. Surprisingly, the microbial communities living underneath meadows do not fully use this sugar stock in their metabolism. Instead, sucrose piles up in the sediments to mM concentrations underneath multiple types of seagrass meadows. Sediment incubation experiments show that microbial communities living underneath a meadow use sucrose at low metabolic rates. Our metagenomic analyses revealed that the distinct community of microorganisms occurring underneath meadows is limited in their ability to degrade simple sugars, which allows these compounds to persist in the environment over relatively long periods of time. Our findings reveal how seagrasses form blue carbon stocks despite the relatively small area they occupy. Unfortunately, anthropogenic disturbances are threatening the long-term persistence of seagrass meadows. Given that these sediments contain a large stock of sugars that heterotopic bacteria can degrade, it is even more important to protect these ecosystems from degradation.

229.0976 [M+H-2H2O]+
PPM:2
Homo sapiens esophagus DESI ()
LNTO22_1_4 - MTBLS385
Resolution: 17μm, 82x80

Description

282.1452 [M+NH4]+
PPM:1.3
Homo sapiens esophagus DESI ()
LNTO22_1_4 - MTBLS385
Resolution: 17μm, 82x80

Description

229.0977 [M+H-2H2O]+
PPM:2.4
Homo sapiens esophagus DESI ()
LNTO29_16_2 - MTBLS385
Resolution: 17μm, 95x101

Description

265.112 [M+H]+
PPM:6.9
Mus musculus Liver MALDI (CHCA)
Salmonella_final_pos_recal - MTBLS2671
Resolution: 17μm, 691x430

Description

A more complete and holistic view on host–microbe interactions is needed to understand the physiological and cellular barriers that affect the efficacy of drug treatments and allow the discovery and development of new therapeutics. Here, we developed a multimodal imaging approach combining histopathology with mass spectrometry imaging (MSI) and same section imaging mass cytometry (IMC) to study the effects of Salmonella Typhimurium infection in the liver of a mouse model using the S. Typhimurium strains SL3261 and SL1344. This approach enables correlation of tissue morphology and specific cell phenotypes with molecular images of tissue metabolism. IMC revealed a marked increase in immune cell markers and localization in immune aggregates in infected tissues. A correlative computational method (network analysis) was deployed to find metabolic features associated with infection and revealed metabolic clusters of acetyl carnitines, as well as phosphatidylcholine and phosphatidylethanolamine plasmalogen species, which could be associated with pro-inflammatory immune cell types. By developing an IMC marker for the detection of Salmonella LPS, we were further able to identify and characterize those cell types which contained S. Typhimurium. [dataset] Nicole Strittmatter. Holistic Characterization of a Salmonella Typhimurium Infection Model Using Integrated Molecular Imaging, metabolights_dataset, V1; 2022. https://www.ebi.ac.uk/metabolights/MTBLS2671.

229.098 [M+H-2H2O]+
PPM:3.7
Homo sapiens esophagus DESI ()
LNTO22_1_9 - MTBLS385
Resolution: 75μm, 89x74

Description

229.0977 [M+H-2H2O]+
PPM:2.4
Homo sapiens esophagus DESI ()
TO31T - MTBLS385
Resolution: 75μm, 56x54

Description

229.0979 [M+H-2H2O]+
PPM:3.3
Homo sapiens esophagus DESI ()
LNTO22_1_7 - MTBLS385
Resolution: 75μm, 69x54

Description

229.0976 [M+H-2H2O]+
PPM:2
Homo sapiens esophagus DESI ()
LNTO30_7_2 - MTBLS385
Resolution: 75μm, 82x68

Description


Phenylacetylglutamine is a product formed from the conjugation of phenylacetate and glutamine. Technically, it is the amino acid acetylation product of phenylacetate (or phenylbutyrate after beta-oxidation). Phenylacetylglutamine is a normal constituent of human urine, but other mammals such as the dog, cat, rat, monkey, sheep, and horse do not excrete this compound. Phenylacetyl-CoA and L-glutamine react to form phenylacetylglutamine and coenzyme A. The enzyme (glutamine N-acetyl transferase) that catalyzes this reaction has been purified from human liver mitochondria and shown to be a polypeptide species distinct from glycine-N-acyltransferase. Phenylacetylglutamine is a major nitrogenous metabolite that accumulates in uremia (PMID: 2791363, 8972626). It has been shown that over 50\\\% of urine phenylacetylglutamine may be derived from kidney conjugation of free plasma phenylacetic acid and/or from the kidneys preferential filtration of conjugated phenylacetic acid (PMID: 6420430). Phenylacetylglutamine is a microbial metabolite found in Christensenellaceae, Lachnospiraceae and Ruminococcaceae (PMID: 26241311). Phenylacetylglutamine is a product formed by the conjugation of phenylacetate and glutamine. Technically it is the amino acid acetylation product of phenylacetate (or phenylbutyrate after beta-oxidation). Phenylacetylglutamine is a normal constituent of human urine, but other mammals including the dog, cat, rat, monkey, sheep and horse do not excrete this compound. Phenylacetyl CoA and glutamine react to form phenylacetyl glutamine and Coenzyme A. The enzyme (Glutamine N-acetyl transferase) that catalyzes this reaction has been purified from human liver mitochondria and shown to be a distinct polypeptide species from glycine-N-acyltransferase. Phenylacetylglutamine is a major nitrogenous metabolite that accumulates in uremia. (PMID: 2791363; PMID: 8972626). It has been shown that over 50\\\% of urine phenylacetylglutamine may be derived from kidney conjugation of free plasma phenylacetic acid and/or from the kidneys preferential filtration of conjugated phenylacetic acid (PMID: 6420430) Phenylacetylglutamine is a colonic microbial metabolite from amino acid fermentation.