Glutamic acid biochemical structure

The number of known or presumed mononuclear, non-heme iron oxygenases and related enzymes continues to grow. This is due to intensive biochemical research and especially based on sequence data derived from genome research projects i.14). For several of these enzymes structural data are available by now from protein crystallography (12-14). In many of the iron oxygenases the iron is facially bound by two histidines and one carboxylate donor, either glutamic acid or aspartic acid. Thus, the term 2-His-l-carboxylate facial triad has been introduced by L. Que Jr. for this motif (19). 

Tetrahydrofolic acid then functions as a carrier of one-carbon groups for amino acid and nucleotide metabolism. The basic ring system is able to transfer methyl, methylene, methenyl, or formyl groups, and it utilizes slightly different reagents as appropriate. These are shown here for convenience, we have left out the benzoic acid-glutamic acid portion of the structure. These compounds are all interrelated, but we are not going to delve any deeper into the actual biochemical relationships. 

Some Compounds Structurally Related to Glutamic Acid. Their Application in Microbiological Determination of Small Quantities of Glutamine. Biochem. J. 42, 485 (1948). 

Normal hemoglobin (HbA) is composed of two a chains and two chains (a2/S2)- The biochemical defect that leads to the development of HbS involves the substitution of valine for glutamic acid as the sixth amino acid in the /3-polypeptide chain. Another type of abnormal hemoglobin, hemoglobin C (HbC), is produced by the substitution of lysine for glutamic acid as the sixth amino acid in the 8-chain. Structurally, the a-chains of HbS, HbA, and HbC are identical. Therefore it is the chemical differences in the /3-chain that explain sickling and its related sequelae. ... 

To imderstand the actions of domoic acid in the nervous system, we must recognize its structural similarities with glutamic acid (see Figure 1). While most people not familiar with nervous system function think of glutamate as a simple amino acid that participates in biochemical pathways (e.g. feeding carbon atoms into the... 

The structural similarity of the 5-carbon amino acids, glutamic acid, ornithine, proline, and hydroxyproline, suggested interrelations in their metabolism very early to biochemical investigators. ... 

To achieve their different effects NTs are not only released from different neurons to act on different receptors but their biochemistry is different. While the mechanism of their release may be similar (Chapter 4) their turnover varies. Most NTs are synthesised from precursors in the axon terminals, stored in vesicles and released by arriving action potentials. Some are subsequently broken down extracellularly, e.g. acetylcholine by cholinesterase, but many, like the amino acids, are taken back into the nerve where they are incorporated into biochemical pathways that may modify their structure initially but ultimately ensure a maintained NT level. Such processes are ideally suited to the fast transmission effected by the amino acids and acetylcholine in some cases (nicotinic), and complements the anatomical features of their neurons and the recepter mechanisms they activate. Further, to ensure the maintenance of function in vital pathways, glutamate and GABA are stored in very high concentrations (10 pmol/mg) just as ACh is at the neuromuscular junction. 

Vitamin M Vitamin M is also called pteroylglutaminic add or folic acid. It was isolated from yeast extract by Wills in 1930. Its structure was described by Anger in 1946. Folic add is made up of pteridine + p-aminobenzoic add + glutamic add. There are several known derivatives, called folates, which are capable of mutual restructuring. The coenzyme tetrahydrofolic acid, which plays a role in many biochemical reactions, is formed with the help of Bi2. Around 50% of total body folate are stored in the liver. A folate-binding protein (FBP) is available for transport. Folate undergoes enterohepatic circulation. The release of folate from the liver cells is stimulated by alcohol, which increases urine excretion. Folate deficiency (e.g. in the case of alcohol abuse) is accompanied by the development of macrocytosis. 

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