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At least 217 records · Page 12Linked to original sources
PubMed1996

Complementarity determining region residues aspartic acid at H55, serine at H95 and tyrosines at H97 and L96 play important roles in the B72.3 antibody-TAG72 antigen interaction.

Structural analysis derived from the crystallographic study of the chimeric B72.3 antibody illustrated some major atomic interactions between complementarity determining region (CDR) residues. For example, hydrogen bonds are formed between H35/H95, L50/H97, H53/H55 and H96/L96 respectively. These CDR residues may play important roles in the B72.3-TAG72 (antibody-antigen) interaction either by direct interaction with the TAG72 antigen or by maintaining a CDR loop conformation through atomic interactions between CDR residues. In order to confirm these assumptions, we altered these CDR residues by site-directed mutagenesis and determined binding affinities of these mutant chimeric antibodies for the TAG72 antigen in a solid-phase radioimmunoassay. We found that H55, H95, H97 and L96 are important CDR residues for the B72.3-TAG72 interaction. Single amino acid substitutions of aspartic acid and serine by alanine at H55 of CDR2 and at H95 of CDR3 respectively and of tyrosine by phenylalanine at H97 and L96 of CDR3, significantly reduced the binding affinity for the TAG72 antigen by 20-, 8-, 16- and 45-fold respectively. Therefore, this study reveals some of the requirements for maintaining the integrity of the B72.3 antibody combining sites.

Amino Acid Sequence↗
PubMed1983

Release of [3H]L-glutamine acid (L-Glu) and [3H]D-aspartic acid (D-Asp) in the area of nucleus tractus solitarius in vivo produced by stimulation of the vagus nerve.

We have investigated the effects of bilateral electrical stimulation of the vagus nerves in anesthetized, paralyzed rats on the release of exogenously administered [3H]L-glutamic acid ([3H]L-Glu) or [3H]D-aspartic acid ([3H]D-Asp) from the intermediate portion of the nucleus tractus solitarius (NTS). Electrical stimulation of afferent fibers with the frequency, pulse, duration, and intensity required to activate C-fibers, elicited hypotension and bradycardia. Such stimuli induced the release of [3H]L-Glu, or its stable analogue [3H]D-Asp, from the NTS into perfusate collected through push-pull cannulae. The release of radioactive materials, calculated as a percent of increase in radioactivity above the prestimulation level, was for [3H]L-Glu 114.4 +/- 25.1% (n = 20) during bilateral vagal stimulation, and 45.6 +/- 11.3% (n = 9) (P less than 0.001) during unilateral stimulation. The release of [3H]D-Asp induced by bilateral vagal stimulation was 100.4 +/- 31.9%. The release, which was anatomically specific and restricted to the NTS, was directly related to stimulus (and hence reflex) intensity. Overflow of the inert substances [14C]urea OR [14C]sucrose, co-administered with the [3H] amino acids, did not increase at the same time. Local depolarization of the cells in the NTS by K+ (53mM) increased the overflow of [3H]L-Glu, as well as [14C]urea, and was able to induce the release of [3H]L-Glu when electrical stimulation failed to have an effect. The results are consistent with the hypothesis that L-Glu is a neurotransmitter of neurons in the NTS mediating vasodepressor response from vagal afferents, including those from systemic baroreceptors.

Animals↗
PubMed1976

The biosynthesis of multi-L-arginyl-poly(L-aspartic acid) in the filamentous cyanobacterium Anabaena cylindrica.

The cyanobacteria produce multi-L-arginyl-poly (aspartic acid), a high molecular weight (Mr=25 000-125 000) branched polypeptide consisting of a poly(aspartic acid) core with L-arginyl residues peptide bonded to each free carboxyl group of the poly(aspartic acid). An enzyme which will elongate Arg-poly(Asp) has been isolated and purified 92-fold from the filamentous cyanobacterium Anabaena cylindrica. The enzyme incorporates arginine and aspartic acid into Arg-poly(Asp) in a reaction which requires ATP, KCl, MgCl2, and a sulfhydryl reagent. The enzymatic incorporation of arginine is dependent upon the presence of L-aspartic acid but not visa versa, a finding which suggests the order of amino acid addition to the branched polypeptide-aspartic acid is added to the core followed by the attachment of an arginine branch. The elongation of Arg-poly(Asp) in-vitro is insensitive to the addition of protein synthesis inhibitors and to the addition of nucleases. These findings support the notion previosly suggested from in-vivo studies that Arg-poly(Asp) is synthesized via a non-ribosomal route and also demonstrate that amino-acetylated transfer-RNAs play no part in at least one step of the biosynthetic mechanism.

Arginine↗
PubMed1999

Mechanism of Ret activation by a mutation at aspartic acid 631 identified in sporadic pheochromocytoma.

Mutations at aspartic acid 631 in Ret were reported in sporadic pheochromocytoma and medullary thyroid carcinoma. We replaced this aspartic acid with four other amino acids including tyrosine, glycine, asparagine, and alanine and investigated the transforming activity of these mutant cDNAs. Among them, RET cDNA with a mutation of aspartic acid to tyrosine (D631Y) that was reported in sporadic pheochromocytoma showed high transforming activity. The D631Y mutation activated Ret by inducing its disulfide-linked dimerization in the transfectant as observed for multiple endocrine neoplasia (MEN) 2A mutations at cysteine 609, 611, 618, 620, 630, or 634. Further mutation analysis suggested that cysteine 630 or 634 could be involved in the disulfide-linked Ret dimerization induced by the D631Y mutation.

3T3 Cells↗
PubMed1983

The effect of morphine, naloxone, D- and L-aspartic acid on the brain and lung ACE in mice.

The brain and lung angiotensin converting enzyme (ACE) activities of the mice injected with 10 mg/kg morphine and/or naloxone, 200 mg/kg D- and/or L-aspartic acid were spectrophotometrically determined. Morphine, naloxone, D- and L-aspartic acid alone inhibited both brain and lung ACE activities whereas the combinations of morphine with naloxone, D-aspartic acid with L-aspartic acid and morphine with naloxone + L-aspartic acid showed no inhibitory effect on the brain ACE. While naloxone or L-aspartic acid partly antagonized the suppression of morphine on the lung ACE their combination completely prevented morphine from inhibiting the lung ACE. In the in vivo experiments performed on the brain and lung homogenates of the untreated mice the determination of the ACE activity in the incubating media containing 3.10(-3) M morphine or naloxone, 10(-2) M D- or L-aspartic acid showed a significant decrease in the activity. But no in vitro antagonistic effect was found by using the combinations of the drugs used in the study. The antagonism seen in the in vivo experiments was considered as an indirect one. And the relationship between the inhibitory effect of morphine, naloxone and D-aspartic acid, their suppressive effect on drinking and their beneficial effects in various forms of shock was discussed.

Animals↗
PubMed2006

Studies on induction of L-aspartic acid modified chitosan to crystal growth of the calcium phosphate in supersaturated calcification solution by quartz crystal microbalance.

Acidic amino acids, such as aspartic acid (L-Asp) and glutamic acid, are the primary bioactive molecules of the glycoprotein on the organic/inorganic interface of biomineralized tissues. In this study, the induction of chitosan film modified with L-Asp on the crystal growth of hydroxyapatite (HAP) was investigated by a novel in situ analysis approach, quartz crystal microbalance (QCM), associated with the dynamically structural and morphological characterization of precipitation products on various phases by X-ray diffraction (XRD), Fourier-transformed infrared (FT-IR) spectroscopy and scanning electron microscopy (SEM). The natural chitosan exhibited no inducing ability on the crystal growth of HAP. However, the growth rate of induced HAP was dramatically accelerated by the L-Asp modification of chitosan film and increased with the increase of the concentration of L-Asp in the chitosan substrate. It was shown that the chelation of calcium ion with L-Asp provided a nucleation centre and the cluster nuclei was formed by adsorbing further PO(4)(3-), Ca(2+), and then HAP deposited on the original HAP coating in the supersaturated calcification solution (SCS). The developed method allows a kinetic evaluation of the induction of organic film on crystal nucleation and the growth of HAP in vitro.

Aspartic Acid↗
PubMed1993

Postmortem estimation of age at death based on aspartic acid racemization in dentin: its applicability for root dentin.

The extent of aspartic acid racemization in total dentin and in dentin protein fractions from the roots of third molars was determined. In several cases coronal dentin was also investigated. The results of other authors, according to which the racemization of aspartic acid in root dentin apparently proceeds differently than in coronal dentin, could be confirmed. Consequently, the data published so far on age determination based on the extent of aspartic acid racemization in coronal dentin and the "entire dentin of longitudinal sections" cannot be applied to root dentin. In total root dentin and the acid soluble protein of root dentin, a close relationship was observed between the extent of aspartic acid racemization and age. Accordingly, estimation of age at death based on aspartic acid racemization in dentin is also possible for root dentin, apparently with good results. This is important particularly in those cases where a large portion of the coronal dentin is absent, for instance following dental treatment. In the investigation of root dentin, regression equations specific for root dentin must be employed in the estimation of age at death. Corresponding equations for third molars were calculated.

Adult↗
PubMed1980

Mass spectrometric technique for the determination of N-phosphonoacetyl-L-aspartic acid in serum.

N-Phosphonoacetyl-L-aspartic acid (PALA), a potent inhibitor of aspartic acid transcarbamylase, is now undergoing Phase I clinical trials. Initial experiments revealed that PALA is not metabolized to phosphonoacetic acid (PAA) in humans. Thus PALA may be quantified in serum after in vitro conversion to PAA. Serum is deproteinized with perchloric acid, lipid extracted with methylene chloride, hydrolyzed with 8 N hydrochloric acid at 100 degrees for 3 h, and evaporated to dryness with nitrogen. The residue is silylated, and PAA is quantified by monitoring the (M + 1)+ ions of the protonated molecular ions of trimethylsilyl derivatives of PAA and phosphonopropionic acid (internal standard) obtained in chemical ionization with methane. Limit of detection is 0.5 microM (150 ng/ml) PALA using 1 ml serum. PALA was given by continuous infusion to cancer patients at various doses. Maximum levels of PALA (50-500 microM range) were obtained at the end of infusion, followed in most cases by biexponential decay. Persistent residual PALA levels (5 microM for 48 h after infusion) correlated with increased toxicity.

Antineoplastic Agents↗
PubMed1982

[Total parenteral nutrition of premature infants: metabolic effects of an exogenous supply of L-aspartic acid and L-glutamic acid].

Within the scope of clinically indicated total parenteral nutrition of premature infants, a comparative randomized study was performed to examine--by means of nitrogen-balance studies and determination of the free amino acids in the serum--the metabolic effects of absent or parallel intake of 1.140 mumol L-aspartic acid plus 2.160 mumol L-glutamic acid per kg body weight per day in complete L-amino acid solutions with a comparative E/T-ratio and with identical intake of all other nutrients adapted to the requirement. 1. The nitrogen balance level was not affected by the absent or parallel intake of the dicarbonic acids. 2. Intravenous intakes of glycine plus L-serine, which are higher than 2.5 mmol per kg body weight and day, caused statistically significant increased serum concentrations of glycine and L-serine. Such intakes are obviously above the physiologic regulation range. 3. The absent intake of L-aspartic acid and L-glutamic acid resulted in parallel, statistically significant reduced serum concentrations of aspartic acid and asparagine as well as in homeostatic serum concentrations of glutamic acid and glutamine. Despite the only 15-20% higher intake of proline, alanine and arginine under the infusion regimen lacking dicarbonic acids, there was a parallel, statistically significant marked increase in the serum concentrations of proline, alanine, arginine and methionine as well as a statistically significant marked decrease in those of taurine. Under the infusion regimen containing dicarbonic acids exclusively, constant homeostatic serum concentrations of these amino acids as well as of aspartic acid and glutamic acid were measured. 4. A direct or indirect effect of the exogenous supply of L-aspartic acid and/or L-glutamic acid on the homeostasis of aspartic acid and asparagine, on the endogenous turnover of L-alanine and L-proline as well as on the physiologic course of the Krebs-Henseleit cycle and of the "transsulfuration pathway" must be discussed. 5. Since the supply rates of L-aspartic acid plus L-glutamic acid chosen in series 2 (when continuously administered during 24-hour periods) apparently do not cause any disturbance in amino-acid homeostasis, it is established that under the nutritional conditions given this intake lies within the respective physiologic regulation range and therefore is atoxic.

Amino Acids↗
PubMed1994

Estimation of age at death based on aspartic acid racemization in noncollagenous bone proteins.

Age at death determination based on the extent of aspartic acid racemization in dentin has been reported to be highly accurate and reproducible. To test the applicability of this method to human bone, aspartic acid racemization in noncollagenous proteins of bone was investigated. A close relationship was found between age at death and the extent of aspartic acid racemization in osteocalcin, the most abundant noncollagenous protein of the organic bone matrix. Our findings indicate that osteocalcin is a permanent, 'aging' constituent of the organic bone matrix whose D-aspartic acid content increases with age because of in vivo racemization. Thus, the extent of aspartic acid racemization in bone osteocalcin is a measure of the age of the peptide and hence of the entire organism. The relationship between age at death and the extent of aspartic acid racemization in purified bone osteocalcin appears to be close enough to serve as a basis for determination of age at death in forensic medicine.

Age Determination by Skeleton↗
PubMed1977

Aspartic acid and glutamic acid levels in the cochlear nucleus after auditory nerve lesion.

Aspartic acid, glutamic acid and alanine were measured in the cochlear nucleus after lesioning the auditory nerve by cochlear ablation. Ultrastructural analysis of the cochlear nucleus showed that most primary auditory terminals were degenerating one day after cochlear ablation; the terminals were enlarged and the number of synaptic vesicles was reduced. Primary auditory terminals were virtually gone three days after cochlear ablation. Aspartic acid decreased after cochlear ablation in parallel with the morphological degeneration of the primary auditory terminals. The level of total aspartic acid in the cochlear nucleus had decreased more than 8% one day after cochlear ablation and more than 30% after two days, and remained at this level up to 28 days. Glutamic acid also decreased in the cochlear nucleus after cochlear ablation but not in parallel with the morphological degeneration of the primary auditory terminals. Following a slight increase one day after cochlear ablation, total glutamic acid decreased about 10% after two days and continued to decrease slowly through to day 28. Alanine dropped slowly after cochlear ablation and not in parallel with the degeneration of the primary terminals. Levels of other amino acids measured were unchanged or had increased two days after cochlear ablation. Aspartic acid and glutamic acid did not decrease in the superficial layers of the dorsal cochlear nucleus, an area receiving little or no primary innervation.

Alanine↗
PubMed1974

Concordance of collagen-based radiocarbon and aspartic-acid racemization ages.

By determining the extent of racemization of aspartic acid in a well-dated bone, it is possible to calculate the in situ first-order rate constant for the interconversion of the L and D enantiomers of aspartic acid. Collagen-based radiocarbon-dated bones are shown to be suitable samples for use in "calibrating" the racemization reaction. Once the aspartic-acid racemization reaction has been "calibrated" for a site, the reaction can be used to date other bones from the deposit. Ages deduced by this method are in good agreement with radiocarbon ages. These results provide evidence that the aspartic-acid racemization reaction is an important chronological tool for dating bones either too old or too small for radiocarbon dating. As an example of the potential application of the technique for dating fossil man, a piece of Rhodesian Man from Broken Hill, Zambia, was analyzed and tentatively assigned an age of about 110,000 years.

Animals↗
PubMed1988

Primary deuterium isotope effects for the 3-methylaspartase-catalyzed deamination of (2S)-aspartic acid, (2S,3S)-3-methylaspartic acid, and (2S,3S)-3-ethylaspartic acid.

3-Methylaspartate ammonia-lyase catalyzes the deamination of (2S)-aspartic acid 137 times more slowly than the deamination of (2S,3S)-3-methylaspartic acid but catalyzes the amination of fumaric acid 1.8 times faster than the amination of mesaconic acid [Botting, N.P., Akhtar, M., Cohen, M. A., & Gani, D. (1988) Biochemistry (preceding paper in this issue)]. In order to understand the mechanistic basis for these observations, the deamination reaction was examined kinetically with (2S)-aspartic acid, (2S,3S)-3-methylaspartic acid, (2S,3S)-3-ethylaspartic acid, and the corresponding C-3-deuteriated isotopomers. Comparison of the double-reciprocal plots of the initial reaction velocities for each of the three pairs of substrates revealed that the magnitude of the primary isotope effect on both Vmax and V/K varied with the substituent at C-3 of the substrate. 3-Methylaspartic acid showed the largest isotope effect (1.7 on Vmax and V/K), 3-ethylaspartic acid showed a smaller isotope effect (1.2 on Vmax and V/K), and aspartic acid showed no primary isotope effect at all. These results, which are inconsistent with earlier reports that there is no primary isotope effect for 3-methylaspartic acid [Bright, H. J. (1964) J. Biol. Chem. 239, 2307], suggest that for both 3-methylaspartic acid and 3-ethylaspartic acid elimination occurs via a predominantly concerted mechanism whereas for aspartic acid an E1cb mechanism prevails.(ABSTRACT TRUNCATED AT 250 WORDS)

Ammonia-Lyases↗