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Validated All-in-One™ qPCR Primer for GAD2(NM_001134366.2) Search again
Product ID:
HQP154128
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
GAD65
Gene Description:
glutamate decarboxylase 2
Target Gene Accession:
NM_001134366.2(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.
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 autoantibody 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
- Molecular mimicry in type 1 diabetes: immune cross-reactivity between islet autoantigen and human cytomegalovirus but not Coxsackie virus.
- The PEVKEK region of the pyridoxal phosphate binding domain of GAD65 expresses a dominant B cell epitope for type 1 diabetes sera
- GAD65-specific B cells and the antibodies they secrete appear to modulate the autoimmune T cell repertoire by down-regulating T cell epitopes in an immunodominant area while boosting epitopes in distant or cryptic regions.
- GAD2 in type 1 diabetes. GAD2 does not play a major role in type 1 diabetes in these two European populations.
- The effect of GAD65 on T-cell activation in stiff-man syndrome and cerebellar ataxia associated with polyendocrine autoimmunity was evaluated.
- The alpha-helical secondary structure of the GAD65 C-terminus must be denatured to generate linear epitopes. The N-terminus is both surface-exposed and linear in the native structure. Masking membrane interactions must be broken for B-cell recognition.
- 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
- dinucleotide repeat polymorphism in GAD65
- results support the hypothesis that presentation of GAD autoantigen by islet endothelium in vivo could promote transmigration of circulating islet autoantigen-specific T-cells primed in regional lymph nodes against islet autoantigens
- GAD antibodies in type I diabetes mellitus has unique N-terminal linear epitopes that are located on the anchoring domain of GAD65 molecules.
- Data suggest that the conversion of full-length glutamate decarboxylase (GAD) to truncated GAD65 mediated by endogenous protease may represent an important mechanism in the regulation of GABA biosynthesis in the brain.
- GAD2 is mapped to chromosome 10p12 and is a candidate gene for human obesity
- The StyI polymorphism in intron 11 of GAD2 did not associate with schizophrenia or suicidal ideation/behavior.
- 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.
- highly heterogeneous recognition of a multitude of INS and GAD65 peptide determinants occurred in the absence of protein recognition, and low functional avidity of the memory T cells
- Among the type 1 diabetes children, increasing neutralising titres was associated positively with increasing antibody levels against GAD65. All siblings with antibodies against GAD 65 had significant titre increase against any of the CBV strains.
- specificity and avidity of GAD65 reactive T-cell clones isolated from patients with type 1 diabetes
- Conformation-dependent autoantibodies directed against GAD65 are markers of Type 1 diabetes.
- GAD65 autoantibody response in the preclinical stage of type 1 diabetes is dynamic and related to the HLA genotypes that confer risk of diabetes.
- Site-directed mutagenesis study validates that cysteine-446 (present in GAD65 as a free sulfhydryl group) plays an important role in GAD65 activity.
- Out of 14 GAD2 markers screened in stage 1, only one met the threshold criteria for follow-up in a range of anxiety disorders and major depression
- marginally significant (0.01 < P < 0.05) associations between four common variants of GAD2 and BMI were observed
- The functional promoter GAD2 -243 A > G variant may influence risk for alcohol dependence (AD) in some populations, or its role may be limited to susceptibility to severe AD.
- DPD-defined epitope specificity is correlated directly with preserved beta-cell functional reserve in GAD65Ab-positive patients and is associated with the milder clinical phenotype of A+B+ KPDM
- We found glutamic acid decarboxylase (Gad65)antibodies in idiopathic generalized epilepsy and type 1 diabetes.
- 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
- GAD2-243A-->G polymorphism in a population of middle-aged White people associates with a modest reduction in body mass index and fasting and oral glucose tolerance test -related plasma glucose levels
- Glutamate cysteine ligase catalytic suunit promoter polymorphisms may influence GAD65 autoantibody levels and influence the age of onset of type 1 diabetes.
- Autoantibodies persist for 6 yearts after diagnosis of latent autoimmune diabetes in adultsbut levels and reactivity to different GAD65 epitopes are not associated with disease progression.
- Differences in the epitope GAD65 binding between mother and child at birth are limited. The epitope pattern at type 1 diabetes diagnosis differed from that at birth, supporting the view that disease-associated epitopes develop between birth and diagnosis
- This study validates LIPS as a robust method to interrogate autoantibodies for the diagnosis of SPS and potentially other neurological diseases.
- The proximity of B- and T-cell epitopes within the GAD65 structure suggests that antigen-antibody complexes may influence antigen processing by accessory cells and thereby T-cell reactivity.
- conclude that masked GAD65Ab are present in the healthy population and that a lack of particular anti-Ids, rather than GAD65Ab per se, is a characteristic of type 1 diabetes.
- We describe using intermittent prednisolone and finding autoantibodies to GAD65 in juvenile neuronal ceroid lipofuscinosis.
- Patients with latent autoimmune diabetes in adults high GAD65(Ab) antibody titers resemble type 1 diabetic patients in their GAD65Ab epitope specificity.