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Validated All-in-One™ qPCR Primer for GAD1(NM_000817.2) Search again
Product ID:
HQP006683
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CPSQ1, DEE89, GAD, SCP
Gene Description:
glutamate decarboxylase 1
Target Gene Accession:
NM_000817.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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.
Gene References into function
- GAD gene transfer into glutamatergic excitatory neurons leading to an inhibitory bias with altered network activity and a neuroprotective phenotype holds potential for treatment of Parkinson's disease
- autoreactivity to GAD25 is rare in newly diagnosed type 1 diabetes and does not underlie GAD67 reactivity
- The activity of GAD was reduced in patients with multiple sclerosis.
- In the human cerebellar cortex some types of 'non-traditional' large neurons are GAD-immunoreactive, in addition to those neurons already known to be GABAergic (i.e., stellate, basket, Purkinje and Golgi neurons).
- The silent C661T substitution in GAD1 did not associated with schizophrenia or suicidal ideation/behavior.
- Single nucleotide polymorphisms of the GAD67 gene are associated with nonsyndromic cleft lip with or without cleft palate.
- Expression of GAD65 and GAD67 mRNA in the (dorsolateral prefrontal cortex) DLPFC and in the occipital cortex was significantly elevated in patients with schizophrenia, whereas the expression of the corresponding proteins and GAT-1 mRNA was unchanged.
- Results describe the effect of phosphorylation on the two well-defined glutamic acid decarboxylase (GAD) isoforms, namely, GAD65 and GAD67, using highly purified preparations of recombinant human brain GAD65 and GAD67.
- Three adjacent SNPs in the 5-prime upstream region of GAD1 showed a positive pairwise association with childhood-onset schizophrenia. Significant transmission distortion of 4-SNP haplotypes was also observed.
- no evidence for significant allelic association between autism and GAD1
- Auto-antibodies to GAD67 and the more widely studied GAD65 homologue encoded by the GAD2 gene, are described in patients with Stiff-Person Syndrome (SPS), epilepsy, cerebellar ataxia and Batten disease.
- Results from the association studies indicate that GAD1 promoter variants are of importance for the Danish bipolar affective disorder.
- Site-directed mutagenesis study validates that cysteine-455 (present in GAD67 as a free sulfhydryl group) plays an important role in GAD67 activity.
- variations in the GAD1 gene may contribute to individual differences in N and impact susceptibility across a range of anxiety disorders and major depression
- GAD67 is localized in the dermis and is potentially involved in variety of skin activities.
- The results indicate that GAD67 mRNA level was reduced by 40% in the autistic group, suggesting that reduced Purkinje cell GABA input to the cerebellar nuclei.
- conclusion is that GAD1 does not play a major role in schizophrenia in the Japanese population
- All 24 children who developed diabetes had high-affinity glutamte decarboxylase autoantibodies before diabetes onset.
- The structure of GAD67 shows a tethered loop covering the active site, providing a catalytic environment that sustains GABA production. In contrast, the same catalytic loop is inherently mobile in GAD65.
- study suggests that the GABRB2 and GAD1 genes individually, as well as the combined effects of the polymorphism in the GAD1, GAD2 and GABRB2 genes, are associated with schizophrenia in the Chinese population
- Subjects with schizophrenia exhibited expression deficits in GAD67.
- GAD67 expression increase was marked in schizophrenics.
- Expression of GAD67 splice variants may be related to human fetal pancreas development.
- Allelic variation in GAD1 (GAD67) is associated with schizophrenia and influences cortical function and gene expression.
- Expression of GAD67 mRNA in basket cells was significantly up-regulated in eight autistic brains compared with that in eight control brains respectively. Stellate cells showed a trend toward a small increase in GAD67 mRNA levels.
- This study validates LIPS as a robust method to interrogate autoantibodies for the diagnosis of SPS and potentially other neurological diseases.
- GAD1 single nucleotide polymorphism is in linkage disequilibrium with a child bipolar I disorder phenotype.
- abruption of GAD1 gene is important to the risk of schizophrenia.
- Data show that the expression of FEZ1,GAD1, and RGS4 are high correlated with one another in the prefrontal cortex of postmortem brain samples.
- Autism may be caused by epigenetic changes in the gene encoding GAD1.
- found evidence of a possible association between GAD67 and oral clefts in Caucasians