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L-alpha-Methylglutamate
?
-
-
-
-
?
L-alpha-methylglutamate + O2
laevulinic acid + NH3
-
-
-
-
?
L-Cysteic acid
?
-
-
-
-
?
L-Cysteine sulfinic acid
?
L-Glu
4-Aminobutanoate + CO2
L-glutamate
4-aminobutanoate + CO2
additional information
?
-
L-Asp
?
-
3-5% of the activity with L-Glu
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-
?
L-Asp
?
-
Phe or 6-azauracil decrease specificity for L-Glu and increase specificity to L-Asp
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-
?
L-Asp
?
-
2% of the activity with L-Glu
-
-
?
L-Cysteine sulfinic acid
?
-
-
-
-
?
L-Cysteine sulfinic acid
?
-
8% of the activity with L-Glu
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
rate-limiting enzyme involved in the synthesis of gamma-aminobutyric acid
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-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
6-azauracil or Phe decrease specificity for L-Glu and increased specificity to L-Asp
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
?
-
isoenzyme GAD2 may play a unique role in nitrogen metabolism
-
-
?
L-Glu
?
-
the enzyme is under the control of the asexual developmental cycle
-
-
?
L-Glu
?
-
production of 4-aminobutanoate, which is the major inhibitory neurotransmitter in the mammalian brain
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
GAD67 is a rate-limiting enzyme for GABA synthesis, GAD65 is important for the local control of GABA synthesis at the synaptic sites, whereas GAD67 is responsible for maintaining GABA baseline levels for both neurotransmitter and metabolite
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
GAD is the rate-limiting enzyme for GABA biosynthesis
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
GAD is the rate-limiting enzyme for GABA biosynthesis
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
ir
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
ir
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
ir
L-glutamate
4-aminobutanoate + CO2
-
-
-
ir
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
alpha-decarboxylation
-
-
?
L-glutamate
4-aminobutanoate + CO2
alpha-decarboxylation
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
the alpha-carboxyl group, leaving as CO2, is thus replaced by a cytoplasmic proton, yielding 4-aminobutanoate
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
ir
L-glutamate
4-aminobutanoate + CO2
-
the reaction does not occur, when L-glutamate concentration is more than 4fold that of L-glutamine
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
664478, 666116, 697040, 697049, 697617, 697841, 698395, 699647, 699674, 700597, 700956, 703503 -
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
GAD is the key enzyme of GABA synthesis, alterations of GABAergic neurotransmission are assumed to play a crucial role in the pathophysiology of mood disorders, overview. Increased relative density of GAD-immunoreactive neuropil, suggests the diathesis of GABAergic system specific for depressed suicidal patients
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-
?
L-glutamate
4-aminobutanoate + CO2
GAD is the rate-limiting enzyme in controlling GABA synthesis, GABA is synthesized by GAD67 is used for the other functions such as trophic factor for neuronal development or energy source. GAD67 is constitutively active and is responsible for the basal GABA production
-
-
?
L-glutamate
4-aminobutanoate + CO2
GAD is the rate-limiting enzyme in controlling GABA synthesis, GAD65 is transiently activated in response to the extra demand of GABA in neurotransmission
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
GAD is the rate-limiting enzyme in neurotransmitter gamma-aminobutyric acid, GABA, biosynthesis
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
human glutamic acid decarboxylase 65 is a key autoantigen in type 1 diabetes
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-
?
L-glutamate
4-aminobutanoate + CO2
-
the isozymes are involved in autoimmune response and diseases, such as diabetes mellitus and Graves' disease, overview. Correlations between anti-GAD autoantibodies and diseases, overview
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-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
ir
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
ir
L-glutamate
4-aminobutanoate + CO2
-
-
-
ir
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
consumption of one H+
-
-
?
L-glutamate
4-aminobutanoate + CO2
the alpha-carboxyl group, leaving as CO2, is replaced by a cytoplasmic proton, yielding 4-aminobutanoate
-
-
?
L-glutamate
4-aminobutanoate + CO2
the alpha-carboxyl group, leaving as CO2, is thus replaced by a cytoplasmic proton, yielding 4-aminobutanoate
-
-
?
L-glutamate
4-aminobutanoate + CO2
irreversible alpha-decarboxylation of L-glutamate in the presence of a pyridoxal 5'-phosphate (PLP) as coenzyme
-
-
ir
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
the alpha-carboxyl group, leaving as CO2, is thus replaced by a cytoplasmic proton, yielding 4-aminobutanoate
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
ir
L-glutamate
4-aminobutanoate + CO2
irreversible alpha-decarboxylation of L-glutamate in the presence of a pyridoxal 5'-phosphate (PLP) as coenzyme
-
-
ir
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
ir
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
the alpha-carboxyl group, leaving as CO2, is replaced by a cytoplasmic proton, yielding 4-aminobutanoate
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
ir
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
consumption of one H+
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
the alpha-carboxyl group, leaving as CO2, is replaced by a cytoplasmic proton, yielding 4-aminobutanoate
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
695988, 697040, 697807, 699924, 700429, 700471, 700474, 700956, 705287, 705316, 705319, 706836 -
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
GAD is the rate-limiting enzyme in controlling GABA synthesis, GABA is synthesized by GAD67 is used for the other functions such as trophic factor for neuronal development or energy source. GAD67 is constitutively active and is responsible for the basal GABA production while GAD65 is transiently activated in response to the extra demand of GABA in neurotransmission
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
GAD is the rate-limiting enzyme in neurotransmitter gamma-aminobutyric acid, GABA, biosynthesis
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
GAD65-mediated GABA synthesis is critical for the consolidation of stimulus-specific fear memory. This function appears to involve a modulation of neural activity patterns in the amygdalo-hippocampal pathway as indicated by a reduction in theta frequency synchronization between the amygdala and hippocampus of Gad65-/- mice during the expression of generalized fear memory
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
GAD67 is the rate-limiting enzyme of GABA biosynthesis
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
nicotine, by activating nAChRs located on cortical or hippocampal GABAergic interneurons, can up-regulate GAD67 expression via an epigenetic mechanism
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
BmGAD can catalyze transformation of glutamate to GABA with a conversion rate of 28.5% (mol/mol) in 4 h at 30°C
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
BmGAD can catalyze transformation of glutamate to GABA with a conversion rate of 28.5% (mol/mol) in 4 h at 30°C
-
-
?
L-glutamate
4-aminobutanoate + CO2
the enzyme also catalyzes the decarboxylation of L-aspartate with slightly higher efficiency. No activity with D-glutamate
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
ir
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
GAD is the rate-limiting enzyme in controlling GABA synthesis, GABA is synthesized by GAD67 is used for the other functions such as trophic factor for neuronal development or energy source. GAD67 is constitutively active and is responsible for the basal GABA production while GAD65 is transiently activated in response to the extra demand of GABA in neurotransmission
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
GAD is the rate-limiting enzyme in neurotransmitter gamma-aminobutyric acid, GABA, biosynthesis
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
glutamate decarboxylase is the rate-limiting enzyme in the synthesis of gamma-aminobutyric acid, the most important inhibitory neurotransmitter in central nervous system
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
the enzyme activity is higher in hippocampus of old rats compared to young rats
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
ir
L-glutamate
4-aminobutanoate + CO2
irreversible alpha-decarboxylation of L-glutamate, the enzyme is highly specific for L-glutamate, no activity with D-glutamate and 23 other amino acids, overview
-
-
ir
L-glutamate
4-aminobutanoate + CO2
irreversible alpha-decarboxylation of L-glutamate
-
-
ir
L-glutamate
4-aminobutanoate + CO2
-
-
-
ir
L-glutamate
4-aminobutanoate + CO2
irreversible alpha-decarboxylation of L-glutamate
-
-
ir
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
ir
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
ir
additional information
?
-
-
no activity with L-aspartate
-
-
?
additional information
?
-
-
the reduction of GAD67 immunoreactive neurons in the hippocampal CA1 region may be closely related to highly susceptibility to memory loss in old aged dogs
-
-
?
additional information
?
-
-
Enterococcus raffinosus strain TCCC11660 has a strong intrinsic GAD activity and shows a high yield of GABA production
-
-
?
additional information
?
-
-
enzyme GAD has a very high substrate specificity. No activity with L-glutamine, L-aspartic acid, L-arginine, L-cysteine, L-alanine, L-glycine, L-histidine, L-lysine, L-methionine, L-valine, L-phenylalanine, L-isoleucine, L-leucine, L-threonine, L-tryptophan, L-tyrosine, L-serine and L-proline. The protein also does not convert D-glutamic acid, indicating that it is strongly enantioselective as well
-
-
?
additional information
?
-
-
Enterococcus raffinosus strain TCCC11660 has a strong intrinsic GAD activity and shows a high yield of GABA production
-
-
?
additional information
?
-
-
enzyme GAD has a very high substrate specificity. No activity with L-glutamine, L-aspartic acid, L-arginine, L-cysteine, L-alanine, L-glycine, L-histidine, L-lysine, L-methionine, L-valine, L-phenylalanine, L-isoleucine, L-leucine, L-threonine, L-tryptophan, L-tyrosine, L-serine and L-proline. The protein also does not convert D-glutamic acid, indicating that it is strongly enantioselective as well
-
-
?
additional information
?
-
-
GadB together with the antiporter gadC constitutes the gad acid resistance system, which confers the ability for bacterial survival for at least 2 h in a strongly acidic environment
-
-
?
additional information
?
-
-
of the two homolous forms of glutamic acid decarboxylase, GAD65 and GAD67, only GAD65 is a common target of autoimmunity
-
-
?
additional information
?
-
-
isoform GAD65 undergoes a side reaction yielding pyridoxamine 5-phosphate, succinic semialdehyde and inactive apo enzyme
-
-
?
additional information
?
-
-
association of the two GAD isoforms in Irish individuals with Alzheimer's disease and relevant alcohol-related traits in the irish affected Sib pair study of alcohol dependence, overview. Significant association of GAD1 with initial sensitivity and age at onset of Alzheimer's disease
-
-
?
additional information
?
-
-
calpains inhibit the GAD cleavage in vivo, overview
-
-
?
additional information
?
-
-
enhanced anti-GAD antibodies are associated with several neurological diseases, possibly also the indiopathic Opsoclonus-myoclonus-ataxia syndrome, OMS. The anti-GAD antibodies might act via impairing GABAergic transmission in specific brainstem and cerebellar circuits, overview
-
-
?
additional information
?
-
-
GAD1 might be the susceptibility gene or another one being the susceptibility gene for autism, located on chromosome 2q31
-
-
?
additional information
?
-
GAD65 plays an essential role in neurotransmission, and is a typical autoantigen in several human autoimmune diseases, such as insulin-dependent diabetes mellitus, IDDM and Stiffman-Person syndrome, SPS. Posttranslational regulation of the enzyme in brain, overview
-
-
?
additional information
?
-
GAD65 plays an essential role in neurotransmission, and is a typical autoantigen in several human autoimmune diseases, such as insulin-dependent diabetes mellitus, IDDM and Stiffman-Person syndrome, SPS. Posttranslational regulation of the enzyme in brain, overview
-
-
?
additional information
?
-
-
high levels of autoantibodies to glutamic acid decarboxylase are associated with the stiff-person syndrome and type 1 diabetes mellitus and other pathologies, immunological analysis and phenotypes, overview
-
-
?
additional information
?
-
-
high titers, and sustained intrathecal synthesis, of antibodies directed against neuronal glutamic acid decarboxylase, GAD, in paraneoplastic as well as non-paraneoplastic limbic encephalitis, phenotype, overview
-
-
?
additional information
?
-
-
isozyme GAD 65 in the stiff person syndrome causes GAD65-specific T cells accumulation in the central nervous system driving the intrathecal GAD65 IgG production, T cells from the cerebrospinal fluid, mechanism, overview. GAD65-specific T cells and clonally expanded GAD65-specific B cells coexist intrathecally, where they may collaborate in the synthesis of GAD65 IgG
-
-
?
additional information
?
-
-
latent autoimmune diabetes in adults, LADA, is a form of type 1 diabetes which is associated with autoimmuno response to the glutamate decarboxylase
-
-
?
additional information
?
-
-
leucoencephalopathy, transverse myelopathy, and peripheral neuropathy in children with cancer are associated with anti-GAD autoantibodies, overview
-
-
?
additional information
?
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the smaller isoform of glutamate decarboxylase, GAD65, is a major autoantigen in type 1 diabetes, antigen presentation of detergent-free glutamate decarboxylase (GAD65) is affected by human serum albumin as carrier protein, immunoresponse analysis, overview
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enzyme activity determination by GABase assay, overview
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enzyme activity determination by GABase assay, overview
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enzyme activity determination by GABase assay, overview
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enzyme/transporter pair GAD2/T2 is primarily responsible for surviving severe acid challenge, enzyme GAD1 plays a major role in growth at mildly acidic pH-values
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enzyme/transporter pair GAD2/T2 is primarily responsible for surviving severe acid challenge, enzyme GAD1 plays a major role in growth at mildly acidic pH-values
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susceptibility of GABAergic neurons or GAD transcript regulation within the context of ischemic injury to neocerebral cortex, overview
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isoform GAD65 plays a major role in gamma-aminobutanoate transmission in normal physiological condition. Isoform GAD67 can serve this role under some pathological conditions
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cortical GABAergic neurons, surviving pathological insult such as ischemia or brain trauma, exposed to glutamate in vitro, display an NMDA receptor-mediated alteration in the levels of the GABA synthesizing enzyme glutamic acid decarboxylase, isozymes GAD65 and 67, mechanism of glutamate excitotoxicity, overview
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GAD65 plays an essential role in neurotransmission, overview
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cortical GABAergic neurons, surviving pathological insult such as ischemia or brain trauma, exposed to glutamate in vitro, display an NMDA receptor-mediated alteration in the levels of the GABA synthesizing enzyme glutamic acid decarboxylase, isozymes GAD65 and 67, mechanism of glutamate excitotoxicity, overview
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enzyme activity detection by rapid pH indicator method. No activity with D-glutamic acid and 2-methyl-DL-glutamic acid
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enzyme activity detection by rapid pH indicator method. No activity with D-glutamic acid and 2-methyl-DL-glutamic acid
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the recombinant engineered enzyme shows a broad substrate specificity
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calpains inhibit the GAD cleavage in vivo, overview
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chronic systemic administration of an agonist of dopamine D1/D5-preferring receptors increases GAD mRNA levels in striatonigral neurons in intact and dopamine-depleted rats. striatal GAD67 mRNA levels were negatively correlated with nigral alpha1 mRNA levels in the dopamine-depleted but not dopamine-intact side. down-regulation of nigral GABAA receptors is linked to the increase in striatal GAD67 mRNA levels in the dopamine-depleted striatum. Different signaling pathways are involved in the modulation by dopamine D1/D5 receptors of GAD65 and GAD67 mRNA levels in striatonigral neurons, overview
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GAD65 plays an essential role in neurotransmission, overview
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regular performance of exercise results in extensive changes in the forebrain GABAergic system that may be implicated in the changes in stress sensitivity and emotionality observed in exercising subjects, overview
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SDF1alpha/CXCR4/G protein/ERK signaling induces the expression of the GAD67 system via Egr1 activation, a mechanism that may promote the maturation of GABAergic neurons during development
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the enzyme is highly substrate specific. No activity with D-glutamate and no activity with L-Asp, L-Ser, L-His, Gly, L-Thr, L-Ala, L-Arg, L-Tyr, L-Cys, L-Val, L-Met, L-Trp, L-Phe, L-Ile, L-Leu, L-Lys, and L-Pro
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the enzyme is highly substrate specific. No activity with D-glutamate and no activity with L-Asp, L-Ser, L-His, Gly, L-Thr, L-Ala, L-Arg, L-Tyr, L-Cys, L-Val, L-Met, L-Trp, L-Phe, L-Ile, L-Leu, L-Lys, and L-Pro
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the activity is closely associated with its developmental status and may represent a link between differentiation events and energy metabolism
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