| InChI=1S/C2H8NO4P/c3-1-2-7-8(4,5)6/h1-3H2,(H2,4,5,6) |
| SUHOOTKUPISOBE-UHFFFAOYSA-N |
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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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Bronsted base
A molecular entity capable of accepting a hydron from a donor (Bronsted acid).
(via organic amino compound )
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human metabolite
Any mammalian metabolite produced during a metabolic reaction in humans (Homo sapiens).
algal metabolite
Any eukaryotic metabolite produced during a metabolic reaction in algae including unicellular organisms like chlorella and diatoms to multicellular organisms like giant kelps and brown algae.
mouse metabolite
Any mammalian metabolite produced during a metabolic reaction in a mouse (Mus musculus).
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View more via ChEBI Ontology
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2-aminoethyl dihydrogen phosphate
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2-amino-ethanol dihydrogen phosphate
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ChEBI
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2-amino-ethanol phosphate
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ChEBI
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colamine phosphate
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ChemIDplus
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colamine phosphoric acid
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ChEBI
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colaminphosphoric acid
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ChEBI
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EAP
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ChEBI
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ethanolamine acid phosphate
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ChEBI
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ethanolamine O-phosphate
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ChEBI
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ethanolamine O-phosphate
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NIST Chemistry WebBook
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Ethanolamine phosphate
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KEGG COMPOUND
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mono(2-aminoethyl) phosphate
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ChemIDplus
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monoaminoethyl phosphate
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ChEBI
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O-phosphocolamine
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NIST Chemistry WebBook
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O-Phosphoethanolamine
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KEGG COMPOUND
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O-Phosphorylethanolamine
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KEGG COMPOUND
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OPE
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ChEBI
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PE
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ChEBI
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PEA
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ChEBI
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PETN
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ChEBI
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pEtN
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ChEBI
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Phosphoethanolamine
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KEGG COMPOUND
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phosphoric acid 2-aminoethyl phenyl ester
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ChEBI
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phosphoryl-ethanolamine
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ChEBI
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1071-23-4
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CAS Registry Number
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ChemIDplus
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1071-23-4
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CAS Registry Number
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NIST Chemistry WebBook
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1758916
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Reaxys Registry Number
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Reaxys
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663022
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Gmelin Registry Number
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Gmelin
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Klunk WE, Debnath ML, McClure RJ, Pettegrew JW (1995)
Inactivity of phosphoethanolamine, an endogenous GABA analog decreased in Alzheimer's disease, at GABA binding sites.
Life sciences 56, 2377-2383 [PubMed:7791524]
[show Abstract]
Phosphoethanolamine (PE) is a metabolite of the phospholipid metabolism which is decreased in Alzheimer's disease brain. PE shows a strong structural similarity to the inhibitory neurotransmitter, GABA, and the GABAB receptor partial agonist, 3-amino-propylphosphonic acid. The ability of PE to compete for binding to GABAA and GABAB binding sites was investigated. GABAA sites were studied using [3H]SR-95531 and [3H]muscimol. GABAB sites were studied using [3H]GABA in the presence of isoguvacine to saturate GABAA sites. Total [3H]GABA binding was also examined. PE showed little activity at any of the GABA binding sites investigated. PE was most potent at GABAB sites, but the IC50 of 7.5 +/- 0.75 mM was considerably higher than its maximal physiologic concentration of approximately 1.5 mM. The efficient exclusion of PE from GABA binding sites may be an important physiologic mechanism in the control of inhibitory neurotransmission. The structural basis for this exclusion is discussed in reference to the GABAB partial agonist 3-amino-propylphosphonic acid. | Doi Y, Kataura A (1975)
Free amino acids in human tonsillar tissue.
Clinical chemistry 21, 414-417 [PubMed:1112054]
[show Abstract]
Free amino acids in the tonsils of 20 individuals were measured column chromatographically. Those always found in readily detectable amounts included O-phosphoserine, taurine, O-phosphoethanolamine, aspartic acid, hydroxyproline, threonine, serine, glutamic acid, proline, glycine, alanine, alpha-amino-n-butyric acid, valine, cystine, methionine, isoleucine, leucine, tyrosine, phenylalanine, ornithine, gamma-amino-butyric acid, lysine, histidine, and arginine. Results were compared for three clinical pathological groups and for four age groups. Some abnormal values may result from the pathological conditions. |
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