Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “GLUTAMIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,351 records · Page 75Linked to original sources
PubMed1994

Immune-related edemagenic activity of glutamines and glutamic acid, components of immunomodulatory agents.

A number of compounds, in their structure similar to the immunomodulatory agent adamantylamide-L-alanyl-D-isoglutamine (AdDP), a desmuramyl analog of muramyl dipeptide (MDP), were compared with respect to their in vivo immunobiological activity. The agents were represented by adamantylamide-peptides or -amino acids differing principally in the nature of glutaminyl moieties. They were all able to induce inflammatory reaction which was prevented by anti-T-cell (TH) mAb, silica, indomethacin and dexamethasone. Responsible for this effect proved to be glutaminyl moieties (glutamine, isoglutamine, or glutamic acid), irrespective of their stereospecificity. Unlike the immunomodulatory molecule of AdDP, neither of the compounds and amino acids were able to stimulate production of antibodies in immunized animals, however.

Adjuvants, Immunologic↗
PubMed1984

Glutamic acid decarboxylase immunoreactivity of olivocochlear neurons in the organ of Corti of guinea pig and rat.

The distribution of glutamic acid decarboxylase (GAD)-like immunoreactivity in the organ of Corti of guinea pig and rat was studied under the light microscope. Indirect immunohistochemical techniques were used. Cochleae were first incubated with a specific antiserum to rat brain GAD and then stained through an avidin-biotin-horseradish peroxidase (HRP) procedure. GAD-like immunoreactivity was visualized as staining with HRP reaction product. Surface preparations were prepared from the immunoreacted cochleae. GAD-like immunoreactivity was found in the inner spiral bundle, tunnel spiral bundle, tunnel crossing fibers, outer hair cell synaptic regions and outer spiral bundles. Little staining was seen in the basal turn. Most of the immunoreactivity was seen in the third and lower fourth turn of the guinea pig cochlea, but even there many efferent fibers and endings were unstained. It is concluded that GAD-like immunoreactivity is present in a subpopulation of cochlear efferents that contains elements from both the medial and the lateral olivocochlear system. Future studies are needed to determine whether this subpopulation is GABA-ergic (i.e. uses gamma-aminobutyric acid as a neurotransmitter) and/or cholinergic.

Animals↗
PubMed2006

Expression of glutamic acid decarboxylase and identification of GABAergic cells in the ischemic rat dentate gyrus.

We have investigated the glutamic acid dexcarboxylase (GAD) mRNA and protein isoforms as markers for ischemic loss of GABAergic neurons in the dentate hilus. Stereological counts of these neurons were performed in rats surviving 8 days after 10 min of transient forebrain ischemia, and in control rats (sham-operated and naïve). GAD65 and GAD67 were detected by both in situ hybridization and immunocytochemistry. No differences (three-way ANOVA, P > 0.05) were found between treatments (ischemia, sham-operated or naïve) when cell counts of identical GAD isoforms were compared at the same level (mRNA or protein). However, irrespective of treatments, the number of neurons expressing GAD65 mRNA was significantly higher than the number of neurons expressing GAD65 protein, and the number of neurons expressing GAD67 mRNA was significantly lower than the number of neurons expressing GAD67 protein. In parallel, we investigated the colocalization of the cell death marker Fluorojade B (FJB) with somatostatin- or GAD67-immunoreactivity in hilus of control and ischemic rats. Although the majority of FJB positive cells also contained somatostatin, a small number of GAD67 immunoreactive neurons contained FJB, suggesting that a small number of GABAergic neurons die after ischemia. In conclusion, this study provides direct evidence that a small proportion of GABAergic hilar neurons succumbs to ischemia. Stereological counts of neurons identified from their expression of either GAD isoform of mRNA or protein revealed a high inter-animal variation at any detection level in both naïve, sham-operated and ischemic rats. Therefore, counts of GABAergic neurons should be carefully interpreted in accordance with the marker used for identification.

Animals↗
PubMed2000

Specific recognition of DNA by integration host factor. Glutamic acid 44 of the beta-subunit specifies the discrimination of a T:A from an A:T base pair without directly contacting the DNA.

Integration host factor (IHF) is a protein that binds to the H' site of bacteriophage lambda with sequence specificity. Genetic experiments implicated amino acid residue Glu(44) of the beta-subunit of IHF in discrimination against substitution of A for T at position 44 of the TTR submotif of the binding site (Lee, E. C., Hales, L. M., Gumport, R. I., Gardner, J. F. (1992) EMBO J., 11, 305-313). We have extended this observation by generating all possible single-base substitutions at positions 43, 44, and 45 of the H' site. IHF failed to bind these H' site substitution mutants in vivo. The K(d)(app) value for each H' site substitution, except for H'45A mutant, was reduced >2000-fold relative to the wild-type site. Substitution of amino acid beta-Glu(44) with alanine prevented IHF from discriminating against the H'44A variant but not the other H' site substitution mutants. Further analysis with other substitutions at position beta44 demonstrated that both oxygens of the wild-type glutamic acid are necessary for discrimination of AT at position 44. Because the beta-Glu(44) residue does not contact the DNA, this residue probably enforces binding specificity indirectly through interaction with amino acids that themselves contact the DNA.

Bacterial Proteins↗
PubMed2000

Molecular analysis of familial androgen insensitivity syndrome due to replacement of glutamic acid 802 by lysine.

We studied a Japanese family presenting at least two cases of complete androgen insensitivity syndrome (CAIS) and negative androgen receptor binding. The index subject showed a 46, XY karyotype and a complete female phenotype. For the purpose of further diagnosis and genetic counseling, molecular analysis of the androgen receptor (AR) gene was performed. Direct sequencing of the AR gene identified a mutation at nucleotide 2935 (A-->G). This replacement was a novel missense mutation, resulting in the substitution of glutamic acid 802 by lysine which deleted a recognition site for EcoRI in exon 6 of the AR gene. We identified another affected individual, using chromosome and molecular analysis of the AR gene at exon 6. Furthermore, although heterozygote carriers could not be identified on clinical grounds, molecular identification of healthy individuals and heterozygote carriers in the family members provided definitive information for genetic counseling. We believe that the molecular analysis of familial CAIS is very informative for both the affected individuals and other family members.

Adolescent↗
PubMedDate not supplied

[Regulation of asparaginase and glutaminase activity in Pseudomonas fluorescens mutants lacking in the ability to synthesize glutamic acid].

A mutant of Pseudomonas fluorescens, AG-M49, has been isolated, which lacks the ability to synthesize glutamic acid. The mutant contains both aspartase A and aspartase AG. The mutant was characterized by a considerably high activity of glutaminase and aspartase, increasing with the rate flow, during its continuous cultivation on a medium with L-glutamate. L-aspartate penetrates the cells and induces formation of the both deamidases in the mutant. In these conditions, the concentration of exocellular ammonia increases. Asparagine, but not glutamine, also stimulates production of the deamidases in the mutant.

Asparaginase↗
PubMed1985

Subcellular distribution of glutamic acid decarboxylase in rat brain regions following electroconvulsive stimulation.

Electroconvulsive stimulation of rats evoked significant increases of glutamic acid decarboxylase (GAD) activity in the synaptosomal fractions of neocortex (including white matter) and hippocampal formation. The elevation of synaptosomal-bound GAD activity was not significant in cingulate cortex, striatum, caudal brainstem and thalamus. The electroconvulsive shocks had no effect on the GAD activity of the cytoplasmic fractions of any brain regions investigated. The highest physiological level of synaptosomal GAD activity was found in thalamus, followed (in decreasing order) by striatum, hippocampus, cingulate cortex, caudal brainstem and neocortex.

Animals↗
PubMed1996

Synthesis, physical properties, toxicological studies and bioavailability of L-pyroglutamic and L-glutamic acid esters of paracetamol as potentially useful prodrugs.

Paracetamol ester prodrugs with L-pyroglutamic and L-glutamic acid, biosynthetic precursors of glutathione, have been synthesized to reduce paracetamol hepatotoxicity and improve bioavailability. The toxicological studies of paracetamol esters show that only L-5-oxo-pyrrolidine-2-paracetamol carboxylate reduces toxicity after administration of an overdose. The glutathione hepatic values in mice obtained by intraperitoneal injection of the ester are superimposable on controls and the oral LD50 was found to be greater than 2000 mg kg-1 and the intraperitoneal LD50 was 1900 mg kg-1. These results taken together with hydrolysis and bioavailability data show that ester is a potential candidate as a prodrug of paracetamol.

Acetaminophen↗
PubMed1997

Detection of a genetic variant, lysine-->glutamic acid at position 372 of human serum albumin, by capillary electrophoresis and structural identification.

A genetic variant of human serum albumin (alloalbumin) is detected by capillary electrophoresis (CE). Two albumin peaks, which were in the ratio of approximately one, were clearly separated. One of the peaks had the same migration time as normal albumin (Alb A) and the other (Alb X) had a longer migration time. SDS-polyacrylamide gel electrophoresis of CNBr fragments (CB) of Alb X indicated that the amino acid substitution was localized in the CB5 fragment (residue 330-446) of the molecule, because of anomalous migration of CB5 in the gel. The CE mapping of the tryptic peptides from the variant CB5 revealed clearly the existence of a new peptide, and the lack of two normal peptides. The sequence analysis of the variant peptide collected by CE micropreparation showed that the N-terminus of the variant peptide corresponded to that of T49 in Alb A. The substitution site, lysine-->glutamic acid at the position 372, was revealed by sequence determination of the variant peptide purified by reversed-phase HPLC.

Amino Acid Sequence↗
PubMed2000

Protein binding of a DRPLA family through arginine-glutamic acid dipeptide repeats is enhanced by extended polyglutamine.

Dentatorubral-pallidoluysian atrophy (DRPLA) is one of the hereditary neurodegenerative disorders caused by expansion of CAG/glutamine repeats. To investigate the normal function of the DRPLA gene and the pathogenic mechanism of neuron death in specific areas of the brain, we isolated and analyzed a gene that shares a notable motif with DRPLA, arginine-glutamic acid (RE) dipeptide repeats. The gene isolated, designated RERE, has an open reading frame of 1566 amino acids, of which the C-terminal portion has 67% homology to DRPLA, whereas the N-terminal portion is distinctive. RERE also contains arginine-aspartic acid (RD) dipeptide repeats and putative nuclear localization signal sequences, but no polyglutamine tracts. RERE is expressed at a low level in most tissues examined. Immunoprecipitation and in vitro binding assays demonstrate that the DRPLA and RERE proteins bind each other, for which one of the RE repeats has a primary role, and extended polyglutamine enhances the binding. With engineered constructs fused with a tag, the RERE protein localized predominantly in the nucleus. Moreover, when RERE is overexpressed, the distribution of endogenous DRPLA protein alters from the diffused to the speckled pattern in the nucleus so as to co-localize with RERE. More RERE protein is recruited into nuclear aggregates of the DRPLA protein with extended polyglutamine than into those of pure polyglutamine. These results reveal a function for the DRPLA protein in the nucleus and the RE repeat in the protein-protein interaction.

Amino Acid Sequence↗
PubMed1989

The coexistence of substance P- and glutamic acid decarboxylase-like immunoreactivity in entopeduncular neurons of the rat.

The coexistence of substance P- and glutamic acid decarboxylase-like immunoreactivity in cell bodies was investigated in the entopeduncular neurons of the rat by the double-immunofluorescence method using species-specific antibodies. Over half of the substance P-like immunoreactive cells were GABAergic. Double-labeled neurons were generally seen in the rostral to the middle region of the entopeduncular nucleus. Since the rostral portion of the entopeduncular nucleus mainly projects to the lateral habenular nucleus, it is suggested that double-labeled neurons in the entopeduncular nucleus largely project to the lateral habenular nucleus which is involved in the limbic system.

Animals↗
PubMed1998

[Antibodies to glutamic acid decarboxylase (GADA) as markers of risk for development of insulin-dependent diabetes mellitus].

Autoantibodies to glutamic acid decarboxylase (GADA)-found frequently before the onset of IDDM are an important marker of the autoimmune process of B cells destruction. The aim of the present study was to evaluate the possible relationship between the frequency of GADA and ICA in first degree relatives of subjects with IDDM. The GADA were determined in 238 first degree relatives of IDDM subjects. In 32 of the investigated subjects GADA were measured second time after 12 months and in 24 of them IVGTT was performed to evaluate FPIR and GADA prevalence relationship. The results demonstrate that combination of ICA and GADA antibodies has a high sensitivity and increases the specificity for predicting IDDM in high risk siblings.

Adolescent↗
PubMed1977

Restriction of primary responses to the IgG class and dependency of IgM responses on secondary immunization for the copolymers of L-glutamic acid, L-tyrosine, and L-alanine.

Primary responses to the linear polymers of L-glutamic acid, L-tyrosine, and L-alanine are restricted to the IgG class of antibodies. The appearance of specific IgM antibodies against these antigens is dependent upon secondary immunization, in contrast to many classical antigenic systems. The presence of an IgM response was verified by a direct plaque-forming cell assay, the inhibition of direct plaques by an antiserum specific for mouse micron-chain, and the physical separation of IgM and IgG GAT-specific antibodies by gel filtration. Preimmunization of the appropriate nonresponder strain with GAT or GT inhibits both the secondary IgM and IgG responses to GAT-MBSA and GT-MBSA, respectively. The tolerance observed is due to the induction of suppressor cells as demonstrated by cell transfer experiments.

Alanine↗
PubMed2001

Potentiation and prolongation of the insulinotropic action of glucagon-like peptide 1 by methyl pyruvate or dimethyl ester of L-glutamic acid in a type 2 diabetes animal model.

Methyl pyruvate and the dimethyl ester of L-glutamic acid were administered intravenously, as a primed constant infusion (1.0-2.0 micromol followed by 0.5-1.0 micromol/min, both expressed per gram of body wt), in adult rats that had been injected with streptozotocin during the neonatal period. Each ester augmented plasma insulin concentration and potentiated and/or prolonged the insulinotropic action of glucagon-like peptide 1 (GLP-1) injected intravenously (5 pmol/g of body wt) at min 5 of the test. It is proposed, therefore, that suitable nonglucidic nutrients, susceptible to bypassing the site-specific defects of D-glucose transport and metabolism responsible for the preferential impairment of the B-cell secretory response to D-glucose in non-insulin-dependent diabetes, could be used to optimize the insulinotropic action of GLP-1.

Animals↗
PubMed1987

Ontogeny of glutamic acid decarboxylase, tyrosine hydroxylase, choline acetyltransferase, somatostatin and substance P in monkey cerebellum.

The enzyme activities of glutamic acid decarboxylase (GAD), tyrosine hydroxylase (TH) and choline acetyltransferase (ChAT) and concentrations of substance P (SP) and somatostatin were determined in the cerebellum of macaque monkey (Macaca fuscata fuscata) at 3 different ages, embryonic 4 months, embryonic 5.5 months (full-term) and adult. Similar graded increases in the activities of GAD and TH were observed during development. In contrast, ChAT activity was relatively high at embryonic 4 months, increased about twofold between embryonic 4 months and 5.5 months, but did not change between embryonic 5.5 months and adult. These findings suggest that noradrenergic terminals develop synchronously with GABAergic interneurons. On the other hand, the innervation by ChAT-containing fibers is completed during the prenatal period. The concentrations of somatostatin and SP were high at embryonic 4 months, and decreased to, respectively, about 1/18 and 1/4 (expressed per g weight) in adult animals. Several interpretations of the decrease of the two neuropeptides in cerebellar tissue during ontogeny are discussed.

Animals↗
PubMedDate not supplied

No specific reactivity to E. coli glutamic acid decarboxylase from sera of newly-diagnosed insulin dependent diabetic patients.

The 65 kD isoform of Glutamic Acid Decarboxylase (GAD), is one of the major autoantigens in human type 1 diabetes mellitus. This enzyme shares amino acid identity, in select regions already determined as antigenic with its counterpart from E. coli. We tested the reactivity of diabetic and normal sera and an E. coli GAD-specific monoclonal antibody (2D9) to E. coli GAD by solid phase and competition ELISA, as well as immunoblotting to check for cross-reactivity of autoantibodies to the two antigens. Specific antibodies for E. coli GAD are present in diabetics and normal subjects without any differences in frequency and titer. The reactivity of such antibodies in ELISA could be blocked in a dose-dependent manner by the addition of excess antigen in the liquid phase. Furthermore, the monoclonal antibody against E. coli GAD does not recognise human recombinant GAD65 in an ELISA. We conclude that there is no basis for cross-reactivity between the two antigens, and antibody reactivity to GAD65 in man cannot arise from cross-reactivity to the E. coli enzyme.

Adolescent↗
PubMed1984

Monosodium glutamate lesions in rat hypothalamus studied by immunohistochemistry for gonadotropin releasing hormone, neurotensin, tyrosine hydroxylase, and glutamic acid decarboxylase and by autoradiography for [3H] estradiol.

Adult male and female rats treated neonatally with monosodium glutamate (MSG) exhibit lesions in the arcuate nucleus of the hypothalamus. Immunohistochemical analysis of the distribution of tyrosine hydroxylase (TH), glutamic acid decarboxylase (GAD), neurotensin (NT) and gonadotropin-releasing hormone (GnRH) reveals substantial destructions of tuberoinfundibular dopamine and NT systems accompanied by a marked reduction of immunoreactivity in the median eminence. GAD immunoreactivity in the arcuate nucleus and median eminence is greatly reduced, while GnRH containing structures in the mediobasal hypothalamus are not noticeably affected. Evaluation of autoradiograms after intravenously administered [3H] estradiol in the ventral hypothalamus indicate an almost complete loss of target neurons in the arcuate nucleus but not in the nearby ventromedial nucleus. The results suggest that: (a) NT- and dopamine-containing neurons of the arcuate nucleus project to the median eminence via tuberoinfundibular NT and dopaminergic pathways; (b) GABA in the median eminence originates to a major extent from neurons of the arcuate nucleus through a tuberoinfundibular GABAergic system; (c) GnRH is produced in the rat outside the arcuate nucleus; (d) the MSG-induced lesion in the basal tuberal region abolishes or strongly diminishes estradiol target neurons in the arcuate nucleus.

Animals↗