4.1.1.15	L-Glu	rate-limiting enzyme involved in the synthesis of gamma-aminobutyric acid	
4.1.1.15	L-Glu	production of 4-aminobutanoate, which is the major inhibitory neurotransmitter in the mammalian brain	
4.1.1.15	L-Glu	isoenzyme GAD2 may play a unique role in nitrogen metabolism	
4.1.1.15	L-Glu	the enzyme is under the control of the asexual developmental cycle	
4.1.1.15	L-glutamate	-	
4.1.1.15	L-glutamate	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	
4.1.1.15	L-glutamate	GAD is the rate-limiting enzyme for GABA biosynthesis	
4.1.1.15	L-glutamate	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	
4.1.1.15	L-glutamate	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	
4.1.1.15	L-glutamate	GAD is the rate-limiting enzyme in controlling GABA synthesis, GAD65 is transiently activated in response to the extra demand of GABA in neurotransmission	
4.1.1.15	L-glutamate	GAD is the rate-limiting enzyme in neurotransmitter gamma-aminobutyric acid, GABA, biosynthesis	
4.1.1.15	L-glutamate	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	
4.1.1.15	L-glutamate	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	
4.1.1.15	L-glutamate	GAD67 is the rate-limiting enzyme of GABA biosynthesis	
4.1.1.15	L-glutamate	glutamate decarboxylase is the rate-limiting enzyme in the synthesis of gamma-aminobutyric acid, the most important inhibitory neurotransmitter in central nervous system	
4.1.1.15	L-glutamate	human glutamic acid decarboxylase 65 is a key autoantigen in type 1 diabetes	
4.1.1.15	L-glutamate	nicotine, by activating nAChRs located on cortical or hippocampal GABAergic interneurons, can up-regulate GAD67 expression via an epigenetic mechanism	
4.1.1.15	L-glutamate	the enzyme activity is higher in hippocampus of old rats compared to young rats	
4.1.1.15	L-glutamate	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	
4.1.1.15	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	
4.1.1.15	additional information	of the two homolous forms of glutamic acid decarboxylase, GAD65 and GAD67, only GAD65 is a common target of autoimmunity	
4.1.1.15	additional information	the activity is closely associated with its developmental status and may represent a link between differentiation events and energy metabolism	
4.1.1.15	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	
4.1.1.15	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	
4.1.1.15	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	
4.1.1.15	additional information	calpains inhibit the GAD cleavage in vivo, overview	
4.1.1.15	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	
4.1.1.15	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	
4.1.1.15	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	
4.1.1.15	additional information	GAD1 might be the susceptibility gene or another one being the susceptibility gene for autism, located on chromosome 2q31	
4.1.1.15	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	
4.1.1.15	additional information	GAD65 plays an essential role in neurotransmission, overview	
4.1.1.15	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	
4.1.1.15	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	
4.1.1.15	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	
4.1.1.15	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	
4.1.1.15	additional information	leucoencephalopathy, transverse myelopathy, and peripheral neuropathy in children with cancer are associated with anti-GAD autoantibodies, overview	
4.1.1.15	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	
4.1.1.15	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	
4.1.1.15	additional information	susceptibility of GABAergic neurons or GAD transcript regulation within the context of ischemic injury to neocerebral cortex, overview	
4.1.1.15	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	
4.1.1.15	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	
4.1.1.15	additional information	Enterococcus raffinosus strain TCCC11660 has a strong intrinsic GAD activity and shows a high yield of GABA production