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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
-
-
-
L-Asp
?
-
Phe or 6-azauracil decrease specificity for L-Glu and increase specificity to L-Asp
-
-
-
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
-
-
-
-
-
L-Glu
4-Aminobutanoate + CO2
-
-
-
-
?
L-Glu
4-Aminobutanoate + CO2
-
rate-limiting enzyme involved in the synthesis of gamma-aminobutyric acid
-
-
?
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
-
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
-
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
-
-
-
-
?
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
-
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
-
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
-
-
?
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
-
-
?
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
-
-
?
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
-
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
-
-
-
?
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
-
-
-
-
?
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
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
consumption of one H+
-
-
?
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
-
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
-
-
-
-
ir
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
-
-
-
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
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
ir
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
?
-
-
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
?
-
-
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
-
-
-
additional information
?
-
-
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
-
-
-
additional information
?
-
-
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
-
-
-
additional information
?
-
-
susceptibility of GABAergic neurons or GAD transcript regulation within the context of ischemic injury to neocerebral cortex, overview
-
-
-
additional information
?
-
-
isoform GAD65 plays a major role in gamma-aminobutanoate transmission in normal physiological condition. Isoform GAD67 can serve this role under some pathological conditions
-
-
-
additional information
?
-
-
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
-
-
-
additional information
?
-
-
GAD65 plays an essential role in neurotransmission, overview
-
-
-
additional information
?
-
-
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
-
-
-
additional information
?
-
-
the recombinant engineered enzyme shows a broad substrate specificity
-
-
-
additional information
?
-
-
calpains inhibit the GAD cleavage in vivo, overview
-
-
-
additional information
?
-
-
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
-
-
-
additional information
?
-
-
GAD65 plays an essential role in neurotransmission, overview
-
-
-
additional information
?
-
-
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
-
-
-
additional information
?
-
-
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
-
-
-
additional information
?
-
-
the activity is closely associated with its developmental status and may represent a link between differentiation events and energy metabolism
-
-
-
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
L-Glu
4-Aminobutanoate + CO2
-
rate-limiting enzyme involved in the synthesis of gamma-aminobutyric acid
-
-
?
L-glutamate
4-aminobutanoate + CO2
additional information
?
-
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
Q4PRC2
-
-
-
?
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
K7WYY0
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
P20228
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
GAD is the rate-limiting enzyme for GABA biosynthesis
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
GAD is the rate-limiting enzyme for GABA biosynthesis
-
-
?
L-glutamate
4-aminobutanoate + CO2
-
-
-
-
?
L-glutamate
4-aminobutanoate + CO2
P69910
-
-
-
?
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
-
-
?
L-glutamate
4-aminobutanoate + CO2
Q05329, Q99259
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
Q05329, Q99259
GAD is the rate-limiting enzyme in controlling GABA synthesis, GAD65 is transiently activated in response to the extra demand of GABA in neurotransmission
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L-glutamate
4-aminobutanoate + CO2
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GAD is the rate-limiting enzyme in neurotransmitter gamma-aminobutyric acid, GABA, biosynthesis
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L-glutamate
4-aminobutanoate + CO2
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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
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?
L-glutamate
4-aminobutanoate + CO2
A9ZM78
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L-glutamate
4-aminobutanoate + CO2
Q03U69
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?
L-glutamate
4-aminobutanoate + CO2
D6PXK5
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?
L-glutamate
4-aminobutanoate + CO2
K4HXK6
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?
L-glutamate
4-aminobutanoate + CO2
K4HXK6
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?
L-glutamate
4-aminobutanoate + CO2
Q03U69
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?
L-glutamate
4-aminobutanoate + CO2
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?
L-glutamate
4-aminobutanoate + CO2
D6PXK5
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?
L-glutamate
4-aminobutanoate + CO2
A9ZM78
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?
L-glutamate
4-aminobutanoate + CO2
A9ZM78
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?
L-glutamate
4-aminobutanoate + CO2
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?
L-glutamate
4-aminobutanoate + CO2
B1B389
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?
L-glutamate
4-aminobutanoate + CO2
B1B389
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?
L-glutamate
4-aminobutanoate + CO2
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?
L-glutamate
4-aminobutanoate + CO2
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?
L-glutamate
4-aminobutanoate + CO2
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?
L-glutamate
4-aminobutanoate + CO2
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?
L-glutamate
4-aminobutanoate + CO2
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?
L-glutamate
4-aminobutanoate + CO2
B2ZX20
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L-glutamate
4-aminobutanoate + CO2
P48318, P48320
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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 while GAD65 is transiently activated in response to the extra demand of GABA in neurotransmission
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L-glutamate
4-aminobutanoate + CO2
-
GAD is the rate-limiting enzyme in neurotransmitter gamma-aminobutyric acid, GABA, biosynthesis
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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
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L-glutamate
4-aminobutanoate + CO2
-
GAD67 is the rate-limiting enzyme of GABA biosynthesis
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?
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
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?
L-glutamate
4-aminobutanoate + CO2
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?
L-glutamate
4-aminobutanoate + CO2
-
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?
L-glutamate
4-aminobutanoate + CO2
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?
L-glutamate
4-aminobutanoate + CO2
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ir
L-glutamate
4-aminobutanoate + CO2
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-
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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 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
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?
L-glutamate
4-aminobutanoate + CO2
-
the enzyme activity is higher in hippocampus of old rats compared to young rats
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?
L-glutamate
4-aminobutanoate + CO2
K7XPX5
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?
L-glutamate
4-aminobutanoate + CO2
Q0GE18
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ir
L-glutamate
4-aminobutanoate + CO2
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ir
L-glutamate
4-aminobutanoate + CO2
M1GCP8
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?
additional information
?
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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
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additional information
?
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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
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additional information
?
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of the two homolous forms of glutamic acid decarboxylase, GAD65 and GAD67, only GAD65 is a common target of autoimmunity
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additional information
?
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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
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additional information
?
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calpains inhibit the GAD cleavage in vivo, overview
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additional information
?
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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
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additional information
?
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GAD1 might be the susceptibility gene or another one being the susceptibility gene for autism, located on chromosome 2q31
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additional information
?
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Q05329
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
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additional information
?
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Q99259
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
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additional information
?
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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
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additional information
?
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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
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additional information
?
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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
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additional information
?
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latent autoimmune diabetes in adults, LADA, is a form of type 1 diabetes which is associated with autoimmuno response to the glutamate decarboxylase
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additional information
?
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leucoencephalopathy, transverse myelopathy, and peripheral neuropathy in children with cancer are associated with anti-GAD autoantibodies, overview
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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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additional information
?
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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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additional information
?
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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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additional information
?
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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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additional information
?
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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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additional information
?
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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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additional information
?
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GAD65 plays an essential role in neurotransmission, overview
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additional information
?
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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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additional information
?
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calpains inhibit the GAD cleavage in vivo, overview
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additional information
?
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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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additional information
?
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GAD65 plays an essential role in neurotransmission, overview
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additional information
?
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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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additional information
?
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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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additional information
?
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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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(4Z,7E)-N,N'-dihydroxy-2,2-dimethyl-5,6-dihydro-2H-benzimidazole-4,7-diimine
(5Z)-2-amino-5-(2-nitrobenzylidene)-1,3-thiazol-4(5H)-one
(E)-pent-2-enoic acid
-
20% inhibition at 0.01 mg/ml
1,4-dioxo-1,2,3,4-tetrahydronaphthalen-2-yl 2,3,4-tri-O-acetylpentopyranoside
1-(2-nitrobenzyl)-1H-indole-3-carbaldehyde
1-Methylimidazole
-
about 85% residual activity at 5 mM, about 77% residual activity at 10 mM, about 65% residual activity at 20 mM
10H-indeno[2,1-e]tetrazolo[1,5-b][1,2,4]triazin-10-one
2,4-bis[2-(4-hydroxyphenyl)propan-2-yl]phenol
2,6-pyridine dicarboxylic acid
-
-
2-(benzylsulfanyl)-3-(morpholin-4-yl)-2,3-dihydronaphthalene-1,4-dione
2-chloro-N-[5-([2-oxo-2-[(4-sulfamoylphenyl)amino]ethyl]sulfanyl)-1,3,4-thiadiazol-2-yl]acetamide
2-hydroxy-2-(2-hydroxy-6-oxocyclohex-2-en-1-yl)-1H-indene-1,3(2H)-dione
2-Methyl-3,4-didehydroglutamic acid
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-
2-thioxo-3-[(E)-(3,3,5-trimethylcyclohexylidene)amino]-1,3-thiazolidin-4-one
2-[(2-chloro-5-nitrobenzoyl)amino]-5-iodobenzoic acid
2-[(3-formyl-1H-indol-1-yl)methyl]benzonitrile
3,3'-(4H-1,2,4-triazole-3,5-diyl)bis(4-nitro-1,2,5-oxadiazole)
3,4,5-Trihydroxybenzoic acid
3,4-dihydroxybenzoic acid
3,4-dihydroxyphenylacetic acid
-
-
3,5-Dihydroxybenzoic acid
3-[(2E)-2-[1-(3,4-dimethoxyphenyl)ethylidene]hydrazinyl]benzoic acid
3-[(E)-(2,6-difluorobenzylidene)amino]-2-thioxo-1,3-thiazolidin-4-one
3-[(E)-(4-methoxybenzylidene)amino]-2-thioxo-1,3-thiazolidin-4-one
4'-deoxypyridoxine-5'-phosphate
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about 60% inhibition of GAD65 at 3.5 mM, GAD67 is hardly affected
4'-O-methylpyridoxine-5'-phosphate
-
decreases activity of GAD65 in unphysiologically high concentrations, about 60% inhibition at 3.5 mM. GAD67 activity is hardly affected
4,4'-(phenylmethanediyl)bis[2-(4-chlorophenyl)-5-methyl-2,4-dihydro-3H-pyrazol-3-one]
4,4'-[(4-hydroxyphenyl)methanediyl]bis(2-heptyl-5-methyl-2,4-dihydro-3H-pyrazol-3-one)
4,5-Dihydroxyisophthalic acid
4-(morpholin-4-yl)naphthalene-1,2-dione
4-(piperidin-1-yl)naphthalene-1,2-dione
4-Aminohex-5-ynoic acid
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-
4-methylimidazole
-
about 75% residual activity at 5 mM, about 70% residual activity at 10 mM, about 58% residual activity at 20 mM
4-nitro-1,6-dihydrobenzo[1,2-d:3,4-d']bis[1,2,3]triazole
4-nitro-7-[[(1-phenyl-1H-tetrazol-5-yl)sulfanyl]methyl]-2,1,3-benzothiadiazole
4-[(1,4-dioxo-1,2,3,4-tetrahydronaphthalen-2-yl)sulfanyl]butanoic acid
5,5'-dithiobis(2-nitrobenzoate)
5,6-dichloro-2,1,3-benzothiadiazole-4,7-diol
5-[(E)-benzylideneamino]-6-[(2-hydroxyethyl)amino]pyrimidine-2,4(1H,3H)-dione
5-[(E)-[[1-(2-chlorobenzyl)-1H-indol-3-yl]methylidene]amino]-1,3-dihydro-2H-benzimidazol-2-one
5-[[5-hydroxy-3-methyl-1-(4-methylphenyl)-1H-pyrazol-4-yl]methylidene]-1,3-diphenyl-2-thioxodihydropyrimidine-4,6(1H,5H)-dione
6,11-dioxo-5a,6,11,11a-tetrahydronaphtho[2',3':4,5][1,3]thiazolo[3,2-a]pyridin-12-ium
9H-indeno[1,2-b][1,2,5]oxadiazolo[3,4-e]pyrazin-9-one
Ag+
58.3% residual activity at 2 mM
Al3+
91.2% residual activity at 2 mM
Aminoethylylisothiouronium bromide
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ATP
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in presence of leupeptin in freshly prepared homogenates. Inhibition of enzyme from homogenates stored without Triton X-100 for 24 h at 4°C
BaCl2
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1 mM, 78% inhibition
beta-Methylene-DL-Asp
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betulinic acid
-
27% inhibition at 0.01 mg/ml
biphenyl-3,3'-dicarbaldehyde
Ca2+
activates at 0.2 mM, slight inhibition above 1 mM
CaCl2
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1 mM, 31% inhibition
CdCl2
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1 mM, 38% inhibition
CH3COOH
57.4% residual activity at 2 mM
Chloroacetamide
-
no inhibition at pH 4.6, marked inhibition at pH 6.0 or higher
CoCl2
62% inhibition at 5mM
CuSO4
93% inhibition at 5mM
cyclosporin A
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up to 0.3 mM, partial inhibition of activity in homogenate, but not in the supernatant obtained after centrifuging the homogenate
Cys
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enzyme from embryos
D-erythro-4-fluoroglutamate
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DL-4-Amino-4-phosphonobutyrate
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DL-alpha-Aminoadipic acid
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DL-alpha-Methylglutamate
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FeCl3
-
1 mM, 65% inhibition
FeSO4
92% inhibition at 5mM
ginsenosides
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23% inhibition at 0.01 mg/ml, ethanol extract of Panax quinquefolius, different glycoside derivatives, overview
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Glutamate gamma-hydroxamate
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weak
isoniazide
isoniazide-induced seizures are mediated primarily through competition with the cofactor pyridoxal 5'-phosphate resulting in the inhibition of GAD activity
Isonicotinic acid hydrazide
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L-Asn
-
inhibits 4% at 1 mM
L-Asp
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inhibits 20% at 1 mM
L-aspartate beta-hydroxamate
-
weak
L-Cysteine hydrochloride
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L-cysteine sulfinic acid
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L-erythro-4-fluoroglutamate
-
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methyl 2-amino-3-oxo-3H-phenothiazine-1-carboxylate
methyl 2-[[(2-methylimidazo[1,2-a]pyridin-3-yl)carbonyl]amino]benzoate
MgCl2
-
1 mM, 46% inhibition
Mn2+
92.6% residual activity at 2 mM
MnSO4
88% inhibition at 5mM
N-(2-hydroxy-1,3-dioxo-2,3-dihydro-1H-inden-2-yl)benzamide
N-[4,7-dioxo-6-(phenylamino)-4,7-dihydro-2,1,3-benzoxadiazol-5-yl]acetamide
N-[4,7-dioxo-6-(piperidin-1-yl)-4,7-dihydro-2,1,3-benzoxadiazol-5-yl]acetamide
naphtho[2',3':4,5]imidazo[1,2-a]pyridine-6,11-dione
Pb(CH3COO)2
-
1 mM, 37% inhibition
PCMB
-
0.1 mM, 68.5% inhibition at pH 4.6, irreversible
reduced glutathione
-
enzyme from embryos
Substituted dicarboxylic acids
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-
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ursolic acid
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; 11.2% inhibition at 0.01 mg/ml
valerenic acid
-
20% inhibition at 0.01 mg/ml
ZnSO4
80.4% inhibition at 5mM
[(1,3-dioxo-1,3-dihydro-2H-isoindol-2-yl)oxy]acetic acid
(4Z,7E)-N,N'-dihydroxy-2,2-dimethyl-5,6-dihydro-2H-benzimidazole-4,7-diimine
-
(4Z,7E)-N,N'-dihydroxy-2,2-dimethyl-5,6-dihydro-2H-benzimidazole-4,7-diimine
-
(4Z,7E)-N,N'-dihydroxy-2,2-dimethyl-5,6-dihydro-2H-benzimidazole-4,7-diimine
;
(4Z,7E)-N,N'-dihydroxy-2,2-dimethyl-5,6-dihydro-2H-benzimidazole-4,7-diimine
-
(5Z)-2-amino-5-(2-nitrobenzylidene)-1,3-thiazol-4(5H)-one
-
(5Z)-2-amino-5-(2-nitrobenzylidene)-1,3-thiazol-4(5H)-one
-
(5Z)-2-amino-5-(2-nitrobenzylidene)-1,3-thiazol-4(5H)-one
;
(5Z)-2-amino-5-(2-nitrobenzylidene)-1,3-thiazol-4(5H)-one
-
1,4-dioxo-1,2,3,4-tetrahydronaphthalen-2-yl 2,3,4-tri-O-acetylpentopyranoside
-
1,4-dioxo-1,2,3,4-tetrahydronaphthalen-2-yl 2,3,4-tri-O-acetylpentopyranoside
-
1,4-dioxo-1,2,3,4-tetrahydronaphthalen-2-yl 2,3,4-tri-O-acetylpentopyranoside
;
1,4-dioxo-1,2,3,4-tetrahydronaphthalen-2-yl 2,3,4-tri-O-acetylpentopyranoside
-
1-(2-nitrobenzyl)-1H-indole-3-carbaldehyde
-
1-(2-nitrobenzyl)-1H-indole-3-carbaldehyde
-
1-(2-nitrobenzyl)-1H-indole-3-carbaldehyde
;
1-(2-nitrobenzyl)-1H-indole-3-carbaldehyde
-
10H-indeno[2,1-e]tetrazolo[1,5-b][1,2,4]triazin-10-one
-
10H-indeno[2,1-e]tetrazolo[1,5-b][1,2,4]triazin-10-one
-
10H-indeno[2,1-e]tetrazolo[1,5-b][1,2,4]triazin-10-one
;
10H-indeno[2,1-e]tetrazolo[1,5-b][1,2,4]triazin-10-one
-
2,4-bis[2-(4-hydroxyphenyl)propan-2-yl]phenol
-
2,4-bis[2-(4-hydroxyphenyl)propan-2-yl]phenol
-
2,4-bis[2-(4-hydroxyphenyl)propan-2-yl]phenol
;
2,4-bis[2-(4-hydroxyphenyl)propan-2-yl]phenol
-
2-(benzylsulfanyl)-3-(morpholin-4-yl)-2,3-dihydronaphthalene-1,4-dione
-
2-(benzylsulfanyl)-3-(morpholin-4-yl)-2,3-dihydronaphthalene-1,4-dione
-
2-(benzylsulfanyl)-3-(morpholin-4-yl)-2,3-dihydronaphthalene-1,4-dione
;
2-(benzylsulfanyl)-3-(morpholin-4-yl)-2,3-dihydronaphthalene-1,4-dione
-
2-chloro-N-[5-([2-oxo-2-[(4-sulfamoylphenyl)amino]ethyl]sulfanyl)-1,3,4-thiadiazol-2-yl]acetamide
-
2-chloro-N-[5-([2-oxo-2-[(4-sulfamoylphenyl)amino]ethyl]sulfanyl)-1,3,4-thiadiazol-2-yl]acetamide
-
2-chloro-N-[5-([2-oxo-2-[(4-sulfamoylphenyl)amino]ethyl]sulfanyl)-1,3,4-thiadiazol-2-yl]acetamide
;
2-chloro-N-[5-([2-oxo-2-[(4-sulfamoylphenyl)amino]ethyl]sulfanyl)-1,3,4-thiadiazol-2-yl]acetamide
-
2-hydroxy-2-(2-hydroxy-6-oxocyclohex-2-en-1-yl)-1H-indene-1,3(2H)-dione
-
2-hydroxy-2-(2-hydroxy-6-oxocyclohex-2-en-1-yl)-1H-indene-1,3(2H)-dione
-
2-hydroxy-2-(2-hydroxy-6-oxocyclohex-2-en-1-yl)-1H-indene-1,3(2H)-dione
;
2-hydroxy-2-(2-hydroxy-6-oxocyclohex-2-en-1-yl)-1H-indene-1,3(2H)-dione
-
2-mercaptoethanol
-
enzyme form I and II from embryos
2-mercaptoethanol
-
1 mM, 79% inhibition
2-oxoglutarate
-
-
2-thioxo-3-[(E)-(3,3,5-trimethylcyclohexylidene)amino]-1,3-thiazolidin-4-one
-
2-thioxo-3-[(E)-(3,3,5-trimethylcyclohexylidene)amino]-1,3-thiazolidin-4-one
-
2-thioxo-3-[(E)-(3,3,5-trimethylcyclohexylidene)amino]-1,3-thiazolidin-4-one
;
2-thioxo-3-[(E)-(3,3,5-trimethylcyclohexylidene)amino]-1,3-thiazolidin-4-one
-
2-[(2-chloro-5-nitrobenzoyl)amino]-5-iodobenzoic acid
-
2-[(2-chloro-5-nitrobenzoyl)amino]-5-iodobenzoic acid
-
2-[(2-chloro-5-nitrobenzoyl)amino]-5-iodobenzoic acid
;
2-[(2-chloro-5-nitrobenzoyl)amino]-5-iodobenzoic acid
-
2-[(3-formyl-1H-indol-1-yl)methyl]benzonitrile
-
2-[(3-formyl-1H-indol-1-yl)methyl]benzonitrile
-
2-[(3-formyl-1H-indol-1-yl)methyl]benzonitrile
;
2-[(3-formyl-1H-indol-1-yl)methyl]benzonitrile
-
3,3'-(4H-1,2,4-triazole-3,5-diyl)bis(4-nitro-1,2,5-oxadiazole)
-
3,3'-(4H-1,2,4-triazole-3,5-diyl)bis(4-nitro-1,2,5-oxadiazole)
-
3,3'-(4H-1,2,4-triazole-3,5-diyl)bis(4-nitro-1,2,5-oxadiazole)
;
3,3'-(4H-1,2,4-triazole-3,5-diyl)bis(4-nitro-1,2,5-oxadiazole)
-
3,4,5-Trihydroxybenzoic acid
-
weak
3,4,5-Trihydroxybenzoic acid
-
-
3,4,5-Trihydroxybenzoic acid
-
-
3,4-dihydroxybenzoic acid
-
weak
3,4-dihydroxybenzoic acid
-
-
3,4-dihydroxybenzoic acid
-
-
3,5-Dihydroxybenzoic acid
-
weak
3,5-Dihydroxybenzoic acid
-
-
3-Mercaptopropionic acid
-
-
3-Mercaptopropionic acid
-
-
3-Mercaptopropionic acid
-
; 43% inhibition at 0.1 mM
3-Mercaptopropionic acid
-
-
3-Mercaptopropionic acid
-
-
3-Mercaptopropionic acid
-
-
3-[(2E)-2-[1-(3,4-dimethoxyphenyl)ethylidene]hydrazinyl]benzoic acid
-
3-[(2E)-2-[1-(3,4-dimethoxyphenyl)ethylidene]hydrazinyl]benzoic acid
-
3-[(2E)-2-[1-(3,4-dimethoxyphenyl)ethylidene]hydrazinyl]benzoic acid
;
3-[(2E)-2-[1-(3,4-dimethoxyphenyl)ethylidene]hydrazinyl]benzoic acid
-
3-[(E)-(2,6-difluorobenzylidene)amino]-2-thioxo-1,3-thiazolidin-4-one
-
3-[(E)-(2,6-difluorobenzylidene)amino]-2-thioxo-1,3-thiazolidin-4-one
-
3-[(E)-(2,6-difluorobenzylidene)amino]-2-thioxo-1,3-thiazolidin-4-one
;
3-[(E)-(2,6-difluorobenzylidene)amino]-2-thioxo-1,3-thiazolidin-4-one
-
3-[(E)-(4-methoxybenzylidene)amino]-2-thioxo-1,3-thiazolidin-4-one
-
3-[(E)-(4-methoxybenzylidene)amino]-2-thioxo-1,3-thiazolidin-4-one
-
3-[(E)-(4-methoxybenzylidene)amino]-2-thioxo-1,3-thiazolidin-4-one
;
3-[(E)-(4-methoxybenzylidene)amino]-2-thioxo-1,3-thiazolidin-4-one
-
4,4'-(phenylmethanediyl)bis[2-(4-chlorophenyl)-5-methyl-2,4-dihydro-3H-pyrazol-3-one]
-
4,4'-(phenylmethanediyl)bis[2-(4-chlorophenyl)-5-methyl-2,4-dihydro-3H-pyrazol-3-one]
-
4,4'-(phenylmethanediyl)bis[2-(4-chlorophenyl)-5-methyl-2,4-dihydro-3H-pyrazol-3-one]
;
4,4'-(phenylmethanediyl)bis[2-(4-chlorophenyl)-5-methyl-2,4-dihydro-3H-pyrazol-3-one]
-
4,4'-[(4-hydroxyphenyl)methanediyl]bis(2-heptyl-5-methyl-2,4-dihydro-3H-pyrazol-3-one)
-
4,4'-[(4-hydroxyphenyl)methanediyl]bis(2-heptyl-5-methyl-2,4-dihydro-3H-pyrazol-3-one)
-
4,4'-[(4-hydroxyphenyl)methanediyl]bis(2-heptyl-5-methyl-2,4-dihydro-3H-pyrazol-3-one)
;
4,4'-[(4-hydroxyphenyl)methanediyl]bis(2-heptyl-5-methyl-2,4-dihydro-3H-pyrazol-3-one)
-
4,5-Dihydroxyisophthalic acid
-
weak
4,5-Dihydroxyisophthalic acid
-
-
4-(morpholin-4-yl)naphthalene-1,2-dione
-
4-(morpholin-4-yl)naphthalene-1,2-dione
-
4-(morpholin-4-yl)naphthalene-1,2-dione
;
4-(morpholin-4-yl)naphthalene-1,2-dione
-
4-(piperidin-1-yl)naphthalene-1,2-dione
-
4-(piperidin-1-yl)naphthalene-1,2-dione
-
4-(piperidin-1-yl)naphthalene-1,2-dione
;
4-(piperidin-1-yl)naphthalene-1,2-dione
-
4-Bromoisophthalic acid
-
-
4-Bromoisophthalic acid
-
-
4-nitro-1,6-dihydrobenzo[1,2-d:3,4-d']bis[1,2,3]triazole
-
4-nitro-1,6-dihydrobenzo[1,2-d:3,4-d']bis[1,2,3]triazole
-
4-nitro-1,6-dihydrobenzo[1,2-d:3,4-d']bis[1,2,3]triazole
;
4-nitro-1,6-dihydrobenzo[1,2-d:3,4-d']bis[1,2,3]triazole
-
4-nitro-7-[[(1-phenyl-1H-tetrazol-5-yl)sulfanyl]methyl]-2,1,3-benzothiadiazole
-
4-nitro-7-[[(1-phenyl-1H-tetrazol-5-yl)sulfanyl]methyl]-2,1,3-benzothiadiazole
-
4-nitro-7-[[(1-phenyl-1H-tetrazol-5-yl)sulfanyl]methyl]-2,1,3-benzothiadiazole
;
4-nitro-7-[[(1-phenyl-1H-tetrazol-5-yl)sulfanyl]methyl]-2,1,3-benzothiadiazole
-
4-[(1,4-dioxo-1,2,3,4-tetrahydronaphthalen-2-yl)sulfanyl]butanoic acid
-
4-[(1,4-dioxo-1,2,3,4-tetrahydronaphthalen-2-yl)sulfanyl]butanoic acid
-
4-[(1,4-dioxo-1,2,3,4-tetrahydronaphthalen-2-yl)sulfanyl]butanoic acid
;
4-[(1,4-dioxo-1,2,3,4-tetrahydronaphthalen-2-yl)sulfanyl]butanoic acid
-
5,5'-dithiobis(2-nitrobenzoate)
-
0.1 mM, 50.3% inhibition at pH 4.6, irreversible
5,5'-dithiobis(2-nitrobenzoate)
-
-
5,5'-dithiobis(2-nitrobenzoate)
-
-
5,5'-dithiobis(2-nitrobenzoate)
-
-
5,6-dichloro-2,1,3-benzothiadiazole-4,7-diol
-
5,6-dichloro-2,1,3-benzothiadiazole-4,7-diol
-
5,6-dichloro-2,1,3-benzothiadiazole-4,7-diol
;
5,6-dichloro-2,1,3-benzothiadiazole-4,7-diol
-
5-[(E)-benzylideneamino]-6-[(2-hydroxyethyl)amino]pyrimidine-2,4(1H,3H)-dione
-
5-[(E)-benzylideneamino]-6-[(2-hydroxyethyl)amino]pyrimidine-2,4(1H,3H)-dione
-
5-[(E)-benzylideneamino]-6-[(2-hydroxyethyl)amino]pyrimidine-2,4(1H,3H)-dione
;
5-[(E)-benzylideneamino]-6-[(2-hydroxyethyl)amino]pyrimidine-2,4(1H,3H)-dione
-
5-[(E)-[[1-(2-chlorobenzyl)-1H-indol-3-yl]methylidene]amino]-1,3-dihydro-2H-benzimidazol-2-one
-
5-[(E)-[[1-(2-chlorobenzyl)-1H-indol-3-yl]methylidene]amino]-1,3-dihydro-2H-benzimidazol-2-one
-
5-[(E)-[[1-(2-chlorobenzyl)-1H-indol-3-yl]methylidene]amino]-1,3-dihydro-2H-benzimidazol-2-one
;
5-[(E)-[[1-(2-chlorobenzyl)-1H-indol-3-yl]methylidene]amino]-1,3-dihydro-2H-benzimidazol-2-one
-
5-[[5-hydroxy-3-methyl-1-(4-methylphenyl)-1H-pyrazol-4-yl]methylidene]-1,3-diphenyl-2-thioxodihydropyrimidine-4,6(1H,5H)-dione
-
5-[[5-hydroxy-3-methyl-1-(4-methylphenyl)-1H-pyrazol-4-yl]methylidene]-1,3-diphenyl-2-thioxodihydropyrimidine-4,6(1H,5H)-dione
-
5-[[5-hydroxy-3-methyl-1-(4-methylphenyl)-1H-pyrazol-4-yl]methylidene]-1,3-diphenyl-2-thioxodihydropyrimidine-4,6(1H,5H)-dione
;
5-[[5-hydroxy-3-methyl-1-(4-methylphenyl)-1H-pyrazol-4-yl]methylidene]-1,3-diphenyl-2-thioxodihydropyrimidine-4,6(1H,5H)-dione
-
6,11-dioxo-5a,6,11,11a-tetrahydronaphtho[2',3':4,5][1,3]thiazolo[3,2-a]pyridin-12-ium
-
6,11-dioxo-5a,6,11,11a-tetrahydronaphtho[2',3':4,5][1,3]thiazolo[3,2-a]pyridin-12-ium
-
6,11-dioxo-5a,6,11,11a-tetrahydronaphtho[2',3':4,5][1,3]thiazolo[3,2-a]pyridin-12-ium
;
6,11-dioxo-5a,6,11,11a-tetrahydronaphtho[2',3':4,5][1,3]thiazolo[3,2-a]pyridin-12-ium
-
9H-indeno[1,2-b][1,2,5]oxadiazolo[3,4-e]pyrazin-9-one
-
9H-indeno[1,2-b][1,2,5]oxadiazolo[3,4-e]pyrazin-9-one
-
9H-indeno[1,2-b][1,2,5]oxadiazolo[3,4-e]pyrazin-9-one
;
9H-indeno[1,2-b][1,2,5]oxadiazolo[3,4-e]pyrazin-9-one
-
AgNO3
-
AgNO3
-
1 mM, 68% residual activity
AgNO3
complete inhibition at 5mM
Asp
-
-
biphenyl-3,3'-dicarbaldehyde
-
biphenyl-3,3'-dicarbaldehyde
-
biphenyl-3,3'-dicarbaldehyde
;
biphenyl-3,3'-dicarbaldehyde
-
carboxymethoxylamine
-
Cd2+
-
-
Chelidamic acid
-
weak
Chelidonic acid
-
-
Cu2+
-
-
Cu2+
strong inhibition at 3 mM
CuCl2
-
CuCl2
-
1 mM, 43% inhibition
D-Glu
-
-
dithiothreitol
-
enzyme from embryos
dithiothreitol
-
1 mM, complete inhibition
DL-Penicillamine
-
-
EDTA
-
1 mM, 77% inhibition
EDTA
91.2% residual activity at 2 mM
EGTA
-
0.5 mM, 20% inhibition
Fe2+
-
-
Glutarate
-
inhibits 42% at 1 mM
Hg2+
-
-
Hg2+
37.7% residual activity at 2 mM
HgCl2
-
0.01 mM, 80.1% inhibition at pH 4.6, irreversible
HgCl2
-
1 mM, 89% inhibition
HgCl2
-
1 mM, 31.5% residual activity
Isophthalic acid
-
-
KI
-
-
KI
-
1 mM, 55% residual activity
L-Glu
-
inhibits 25% at 1 mM
L-Glu
-
substrate inhibition at high concentrations
Mercaptosuccinic acid
-
-
Mercaptosuccinic acid
-
-
methyl 2-amino-3-oxo-3H-phenothiazine-1-carboxylate
-
methyl 2-amino-3-oxo-3H-phenothiazine-1-carboxylate
-
methyl 2-amino-3-oxo-3H-phenothiazine-1-carboxylate
;
methyl 2-amino-3-oxo-3H-phenothiazine-1-carboxylate
-
methyl 2-[[(2-methylimidazo[1,2-a]pyridin-3-yl)carbonyl]amino]benzoate
-
methyl 2-[[(2-methylimidazo[1,2-a]pyridin-3-yl)carbonyl]amino]benzoate
-
methyl 2-[[(2-methylimidazo[1,2-a]pyridin-3-yl)carbonyl]amino]benzoate
;
methyl 2-[[(2-methylimidazo[1,2-a]pyridin-3-yl)carbonyl]amino]benzoate
-
Mg2+
90.1% residual activity at 2 mM
N-(2-hydroxy-1,3-dioxo-2,3-dihydro-1H-inden-2-yl)benzamide
-
N-(2-hydroxy-1,3-dioxo-2,3-dihydro-1H-inden-2-yl)benzamide
-
N-(2-hydroxy-1,3-dioxo-2,3-dihydro-1H-inden-2-yl)benzamide
;
N-(2-hydroxy-1,3-dioxo-2,3-dihydro-1H-inden-2-yl)benzamide
-
N-[4,7-dioxo-6-(phenylamino)-4,7-dihydro-2,1,3-benzoxadiazol-5-yl]acetamide
-
N-[4,7-dioxo-6-(phenylamino)-4,7-dihydro-2,1,3-benzoxadiazol-5-yl]acetamide
-
N-[4,7-dioxo-6-(phenylamino)-4,7-dihydro-2,1,3-benzoxadiazol-5-yl]acetamide
;
N-[4,7-dioxo-6-(phenylamino)-4,7-dihydro-2,1,3-benzoxadiazol-5-yl]acetamide
-
N-[4,7-dioxo-6-(piperidin-1-yl)-4,7-dihydro-2,1,3-benzoxadiazol-5-yl]acetamide
-
N-[4,7-dioxo-6-(piperidin-1-yl)-4,7-dihydro-2,1,3-benzoxadiazol-5-yl]acetamide
-
N-[4,7-dioxo-6-(piperidin-1-yl)-4,7-dihydro-2,1,3-benzoxadiazol-5-yl]acetamide
;
N-[4,7-dioxo-6-(piperidin-1-yl)-4,7-dihydro-2,1,3-benzoxadiazol-5-yl]acetamide
-
Na2SO4
-
Na2SO4
10% inhibition at 5mM
NaCl
61.5% inhibition at 10 mM
naphtho[2',3':4,5]imidazo[1,2-a]pyridine-6,11-dione
-
naphtho[2',3':4,5]imidazo[1,2-a]pyridine-6,11-dione
-
naphtho[2',3':4,5]imidazo[1,2-a]pyridine-6,11-dione
;
naphtho[2',3':4,5]imidazo[1,2-a]pyridine-6,11-dione
-
NEM
-
no inhibition at pH 4.6, marked inhibition at pH 6.0 or higher
p-hydroxymercuribenzoate
-
-
p-hydroxymercuribenzoate
-
-
SDS
-
1 mM, 26% inhibition
SDS
66.9% residual activity at 40 mM
Zn2+
-
weak
ZnCl2
-
ZnCl2
-
1 mM, 37% inhibition
[(1,3-dioxo-1,3-dihydro-2H-isoindol-2-yl)oxy]acetic acid
-
[(1,3-dioxo-1,3-dihydro-2H-isoindol-2-yl)oxy]acetic acid
-
[(1,3-dioxo-1,3-dihydro-2H-isoindol-2-yl)oxy]acetic acid
;
[(1,3-dioxo-1,3-dihydro-2H-isoindol-2-yl)oxy]acetic acid
-
additional information
-
inhibitor screening, overview
-
additional information
inhibitor screening, overview
-
additional information
inhibitor screening, overview
-
additional information
-
the glutamate decarboxylase activity of p42 is not inhibited by high concentrations of Mn2+
-
additional information
-
ionomycin inhibits the expression of the full-length enzyme, but not of the truncated mutant, while mu-calpain and calpastatin inhibit the truncated enzyme, but not the full-length wild-type enzyme in the synaptosome, overview
-
additional information
-
enzyme inhibition by glutamic acid decarboxylase autoantibodies, overview
-
additional information
-
aasiaticoside does not inhibit GAD activity even at the highest dose of 0.03 mg/ml. Allylglycine does not inhibit GAD activity even at the highest dose of 0.1 mM; asiaticoside does not inhibit GAD activity even at the highest dose of 0.03 mg/ml, allylglycine exhibits no enzyme inhibition even at the highest dose of 0.1 mM; minor inhibition is seen with the ethanol extract of Panax quinquefolius (23%), betulinic acid (27%), and valerenic acid (20%); minor inhibition is seen with the ethanol extract of Panax quinquefolius (ginsenosides) (23%)
-
additional information
-
identification of inhibitory antibodies, overview
-
additional information
-
under acidic conditions, glutamate/4-aminobutanoate antiport is impaired in minimal media but not in rich ones
-
additional information
-
-
-
additional information
-
glutamate reduces the expression of isozymes GAD65 and GAD67, glutamate's suppressing effect on GAD protein isoforms is significantly attenuated by preincubation with the cysteine protease inhibitor N-acetyl-L-leucyl-L-leucyl-L-norleucinal via blockade of calpain and cathepsin protease activities, overview
-
additional information
-
downregulation of reelin and GAD67 expression by the increase of DNA-methyltransferase 1-mediated hypermethylation of promoters in GABAergic interneurons of the telencephalon
-
additional information
inhibitor screening, overview; inhibitor screening, overview
-
additional information
inhibitor screening, overview; inhibitor screening, overview
-
additional information
-
ionomycin inhibits the expression of the full-length enzyme, but not of the truncated mutant, while mu-calpain and calpastatin inhibit the truncated enzyme, but not the full-length wild-type enzyme in the synaptosome, overview
-
additional information
-
chronic mild stress leads to 60% reduced enzyme activity in old rats, which is reversible by neuronal nitric oxide synthase inhibitor 7-nitroindazole, overview
-
additional information
inhibitor screening, overview
-
additional information
-
inhibitor screening, overview
-
additional information
poor inhibition by LiCl, CaCl2, and KCl. MgCl2 and NaCl have no effect on enzyme activity
-
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Enzyme Nomenclature
New: Word Map on EC 4.1.1.15
COMMENTARY
4.1.1.15-RECOMMENDED NAME
----REACTION TYPE
-3980, 654404, 655357, 656303, 656337, 656454, 656697, 682084, 691484, 692644, 697040, 697049, 697424, 697426, 697564, 697572, 697841, 698535, 699151, 699668, 699674, 700597, 700978, 703503--
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