Glutamate Decarboxylase 1 (Brain, 67kDa) Protéines (GAD1)

Human Glutamate Decarboxylase 1 (Brain, 67kDa) (GAD1) interaction partners

1. In conclusion, this study demonstrates the functional impact of c.391 A > G variant and its biological effect makes it a good candidate as risk variant for schizophrenia.

2. findings of this study provide some evidence that the NPSR1 and GAD1 polymorphisms might play a role in the development of war-related PTSD and its related psychological expressions; further research is needed to elucidate the interactions of specific gene variants and environmental factors in the development of PTSD

3. Association between GAD1 rs3749034 polymorphisms with antisaccade task performance in schizophrenic patients.

4. This study detected significant reductions in the mRNAs associated with GAD1 in the frontal cortex (FC) of autism spectrum disorder.

5. Our results demonstrate a weak effect of the GAD1 gene on the risk of bipolar illness, and the associated marker might represent a proxy for real signals of rare variants.

6. findings converge on variation in glutamic acid decarboxylase 1 gene predicting a susceptibility mechanism that affects white matter fractional anisotropy, GABAergic inhibitory neurotransmission in the dorsolateral prefrontal cortex, and working memory performance.

7. Results show how epigenetic changes in GAD1 expression alter local glutamate metabolism in the brain metastatic microenvironment, contributing to a metabolic adaption that facilitates metastasis outgrowth in that setting.

8. We investigate the possible influence of GAD1 SNPs rs3749034 and rs11542313 on ADHD susceptibility. The C allele of rs11542313 was significantly overtransmitted from parents to ADHD probands. Hyperactive/impulsive score was higher in rs3749034G allele and rs11542313C allele carriers. GAD1 haplotypes were associated with higher hyperactive/impulsive scores in ADHD youths. GAD1 gene is associated with ADHD susceptibility.

9. GAD1 is reactivated by DNA methylation, which provided a model for DNA methylation and the active orchestration of oncogenic gene expression by CTCF in cancer cells.

10. There was no difference in GAD25 and GAD67 gene expression level, and GAD25/GAD67 ratio between patients with first episode psychosis and healthy controls

11. Genetic variability in GAD1 and GAD2 contributes to the risk of methamphetamine dependence in the Thai population.

12. Reduced GAD67 expression in PV neurons is not an upstream cause of the lower levels of GABA-associated transcripts, or of the characteristic behaviors, in schizophrenia.

13. Glutamic acid decarboxylase 67 (GAD67) is one of the isoforms that catalyze GABA synthesis. Here, we used recombinant herpes simplex virus (HSV-1) vectors that encode gad1 gene to evaluate the therapeutic potential of GAD67 in peripheral HIV gp120-induced neuropathic pain

14. This study showed that in female groups, the expression of GABRA5 was generally higher in schizophrenia cases compared to the control.

15. GAD autoantibodies were associated with risk of developing type 1 diabetes.

16. Conversion of GAD autoantibody is associated with patients with presumed type 2 diabetes.

17. The GAD65-independent mechanism for targeting of GAD67 to synaptic vesicles in neurons is not functional in islet beta-cells.

18. These results suggest a link between altered inhibitory mechanisms and synchrony and, therefore point to potential mechanisms via which a disruption in neurodevelopmental processes might lead to pathophysiology associated with schizophrenia.

19. Gene ransfer of GAD67 by herpes simplex virus vectors prevents HIV gp120/ddC-induced neuropathic pain.

20. Phosphate-activated glutaminase and GAD65/67 concentrations are compared in Alzheimer's disease cerebellum versus normal cerebellum controls

Cow (Bovine) Glutamate Decarboxylase 1 (Brain, 67kDa) (GAD1) interaction partners

1. These results suggest that the GAD1 gene is a strong candidate gene that affects growth traits in cattle.

Arabidopsis thaliana Glutamate Decarboxylase 1 (Brain, 67kDa) (GAD1) interaction partners

1. mutations in the two lobes affect GAD1 activation in similar ways and only intact AtCaM1 can fully activate GAD1. Taken together, our data provide new insights into the CaM lobes role in interactions between CaM and plant GAD.

2. Insertion mutants of GAD1 revealed that GABA levels in roots were drastically reduced compared with those in the wild type.

3. Antibody titers to this enzyme identify two subgroups of patients with adult-onset autoimmune diabetes having distinct clinical, autoimmune, and genetic features.

4. Calmodulin activates Gad1 in a unique way by relieving two C-terminal autoinhibition domains of adjacent active sites, forming a 393 kDa Gad1-calmodulin complex with an unusual 1:3 stoichiometry.

Mouse (Murine) Glutamate Decarboxylase 1 (Brain, 67kDa) (GAD1) interaction partners

1. An increase in Gad67 expression is detected in the anterior cingulate cortex of nFabp3 knock-out mice.

2. Gad1 knockout mice showed a reduction of tissue GABA in the hippocampus and cortex including mPFC, and exhibited a cluster of effort-based behavior deficits including decreased home-cage wheel running and increased immobility in both tail suspension and forced swim tests. Results suggest that cortical GABA reduction preferentially impairs the effort-based behavior which requires much effort with little benefit.

3. Glutamic acid decarboxylase 67 (GAD67) is encoded by the GAD1 gene and is one of the two GAD proteins responsible for the synthesis of the neurotransmitter gamma aminobutyric acid (GABA) from glutamate.

4. Our results demonstrate that GAD67 plays an important role in Alzheimer's disease pathology

5. Results suggest age-dependent decrease of GAD65/67 mRNAs but normal densities of certain GABAergic interneurons in the Shank3 transgenic mice.

6. GABA is the major inhibitory neurotransmitter in the brain. We show that Dlx1/Dlx2 homeobox genes regulate GABA synthesis during forebrain development through direct activation of glutamic acid decarboxylase enzyme isoforms that convert glutamate to GABA.

7. These findings reveal that Th and Gad1 share a transcription regulatory mechanism that facilitates odorant-dependent regulation of dopamine and GABA expression levels.

8. Study describes in detail a population of choline acetyltransferase immunoreactive /glutamate decarboxylase 67 neurons predominantly ventral to the central canal of the cervical, thoracic and lumbar spinal cord of adult and juvenile mice. These cells potentially correspond to a sub-population of the cholinergic central canal cluster cells which may play a unique role in controlling spinal cord circuitry.

9. This study demonstrated that Alterations in hypoglossal motor neurons due to GAD67 deficiency in mice.

10. Treadmill running prevented partial sciatic nerve ligation-induced reductions in GAD65/67 production, and, thus, GABA levels may be retained in interneurons and neuropils in the superficial dorsal horn.

11. Gad1 knockdown mice have pronounced sensorimotor gating deficits, increased novelty-seeking and reduced fear extinction

12. Glutamate decarboxylase expression may be a reliable proxy of altered GABAergic transmission.

13. Activity deprivation due to TTX preferentially down-regulated GAD67. BDNF-induced increase in the GAD67 protein was markedly lower than that of GAD65, indicating that BDNF differentially regulates activity-dependent gene expression of the 2 isoforms.

14. The results of this study indicated that the mice heterozygous for GAD67 deficiency primarily in PV neurons share several neurochemical and behavioral abnormalities with schizophrenia.

15. Data demonstrate that GAD67 levels directly influence synaptic inhibition.

16. The GAD65-independent mechanism for targeting of GAD67 to synaptic vesicles in neurons is not functional in islet beta-cells.

17. Results indicate the significant contribution of not only GAD65, GAD67 and VGAT-mediated GABAergic but also glycinergic transmissions to both palate and abdominal wall formations

18. These findings provide original evidence that striatal Gad67 expression is involved in the modulation of learning and social behavior.

19. Analysis of GAD65/67 single and double knock-out embryos revealed that the two GADs play complementary (inhibitory) roles in GnRH migration ultimately modulating the speed and/or direction of GnRH migration.

20. Study reports the identification and characterization of novel GAD1 splicing isoforms, showing GAD1 gene in mouse brain is extensively regulated at the level of transcription

Zebrafish Glutamate Decarboxylase 1 (Brain, 67kDa) (GAD1) interaction partners

1. relative expression domains of the dlx and gad1 genes in the zebrafish telencephalon and diencephalon

2. High levels of GAD67 mRNA were observed in the intermediate and ventral parts of the medial pallium

3. the distribution of GAD67-expressing cells highly resembles the distribution of gamma-aminobutyric acid (GABA)/GAD67-expressing cells found in the early zebrafish (teleost) forebrain, suggesting a prosomeric fate map of GABAergic cell populations

Guinea Pig Glutamate Decarboxylase 1 (Brain, 67kDa) (GAD1) interaction partners

1. Sodium salicylate can regulate differently ABR threshold and expression of glutamic acid decarboxylase in spiral ganglion of juvenile and adult guinea pigs.