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GAD1 encodes one of several forms of glutamic acid decarboxylase, identified as a major autoantigen in insulin-dependent diabetes. Additionally we are shipping GAD Antibodies (205) and GAD Kits (50) and many more products for this protein.
Showing 8 out of 13 products:
This study detected significant reductions in the mRNAs associated with GAD1 in the frontal cortex (FC) of autism spectrum disorder.
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.
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.
Results show how epigenetic changes in GAD1 expression alter local glutamate (show GRIN1 Proteins) metabolism in the brain metastatic microenvironment, contributing to a metabolic adaption that facilitates metastasis outgrowth in that setting.
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.
GAD1 is reactivated by DNA methylation (show HELLS Proteins), which provided a model for DNA methylation (show HELLS Proteins) and the active orchestration of oncogenic gene expression by CTCF (show CTCF Proteins) in cancer cells.
There was no difference in GAD25 and GAD67 gene expression level, and GAD25/GAD67 ratio between patients with first episode psychosis and healthy controls
Genetic variability in GAD1 and GAD2 (show GAD2 Proteins) contributes to the risk of methamphetamine dependence in the Thai population.
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.
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 (show ITIH4 Proteins)-induced neuropathic pain
These results suggest that the GAD1 gene is a strong candidate gene that affects growth traits in cattle.
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.
Insertion mutants of GAD1 revealed that GABA levels in roots were drastically reduced compared with those in the wild type.
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.
Our results demonstrate that GAD67 plays an important role in Alzheimer's disease pathology
Results suggest age-dependent decrease of GAD65/67 mRNAs but normal densities of certain GABAergic interneurons in the Shank3 transgenic mice.
GABA is the major inhibitory neurotransmitter in the brain. We show that Dlx1/Dlx2 homeobox (show PRRX1 Proteins) genes regulate GABA synthesis during forebrain development through direct activation of glutamic acid decarboxylase enzyme isoforms that convert glutamate (show GRIN1 Proteins) to GABA.
These findings reveal that Th and Gad1 share a transcription regulatory mechanism that facilitates odorant-dependent regulation of dopamine and GABA expression levels.
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.
This study demonstrated that Alterations in hypoglossal motor neurons due to GAD67 deficiency in mice.
Treadmill running prevented partial sciatic nerve ligation-induced reductions in GAD65 (show GAD2 Proteins)/67 production, and, thus, GABA levels may be retained in interneurons and neuropils in the superficial dorsal horn.
Gad1 knockdown mice have pronounced sensorimotor gating deficits, increased novelty-seeking and reduced fear extinction
Glutamate decarboxylase (show GLUL Proteins) expression may be a reliable proxy of altered GABAergic transmission.
Activity deprivation due to TTX preferentially down-regulated GAD67. BDNF (show BDNF Proteins)-induced increase in the GAD67 protein was markedly lower than that of GAD65 (show GAD2 Proteins), indicating that BDNF (show BDNF Proteins) differentially regulates activity-dependent gene expression of the 2 isoforms.
relative expression domains of the dlx and gad1 genes in the zebrafish telencephalon and diencephalon
High levels of GAD67 mRNA were observed in the intermediate and ventral parts of the medial pallium
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
Sodium salicylate can regulate differently ABR threshold and expression of glutamic acid decarboxylase in spiral ganglion of juvenile and adult guinea pigs.
This gene encodes one of several forms of glutamic acid decarboxylase, identified as a major autoantigen in insulin-dependent diabetes. The enzyme encoded is responsible for catalyzing the production of gamma-aminobutyric acid from L-glutamic acid. A pathogenic role for this enzyme has been identified in the human pancreas since it has been identified as an autoantigen and an autoreactive T cell target in insulin-dependent diabetes. This gene may also play a role in the stiff man syndrome. Deficiency in this enzyme has been shown to lead to pyridoxine dependency with seizures. Alternative splicing of this gene results in two products, the predominant 67-kD form and a less-frequent 25-kD form.
67 kDa glutamic acid decarboxylase
, glutamate decarboxylase 1
, glutamate decarboxylase 67 kDa isoform
, glutamic acid decarboxylase
, glutamate decarboxylase, 67 kDa isoform
, glutamic acid decarboxylase 1
, glutamate decarboxylase 67
, GLUTAMATE DECARBOXYLASE, 67 KD ISOFORM (GAD-67) (67 KD GLUTAMIC ACID DECARBOXYLASE)
, Glutamate decarboxylase 1 (brain)
, glutamate decarboxylase 1 variant GAD67NT