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GAD2 encodes one of several forms of glutamic acid decarboxylase, identified as a major autoantigen in insulin-dependent diabetes. Additionally we are shipping GAD65 Antibodies (229) and GAD65 Proteins (18) and many more products for this protein.
Showing 9 out of 31 products:
Results describe the gross distribution patterns of GAD65 in human and rhesus monkey thalami and show that they are nearly identical.
GAD65 mRNA was found in the periaqueductal gray.
healthy donor NK cells showed similar degranulation against both GAD65 AA 114-122 pulsed and unpulsed APCs (show APCS ELISA Kits). The pathogenetic significance of the CD3 (show CD3 ELISA Kits)-CD8dullCD56+ 'memory-like NK cell subset' with increased response upon secondary challenge in diabetics remains to be elucidated
Genetic variability in GAD2 and GAD1 contributes to risk of methamphetamine dependence in the Thai population.
Study propose that aberrant accumulation of immunogenic GAD65 in Golgi membranes facilitates inappropriate presentation to the immune system after release from stressed and/or damaged beta-cells, triggering autoimmunity.
UV exposed hydrogen peroxide produces hydroxyl radical that may cause protein damage (GAD-65) to the extent of generating neo-epitopes on the molecule, making it immunogenic.
we investigated the relationship between serum glutamic acid decarboxylase (GAD (show GAD ELISA Kits)) autoantibody (Ab) levels and single nucleotide polymorphisms (SNPs) of the glutamic acid de-carboxylase 2 (GAD2) 5'-untranslated region
GAD (show GAD1 ELISA Kits) autoantibodies were associated with risk of developing type 1 diabetes.
Kaplan-Meier survival curves estimated a worst pancreas graft survival for patients with positive IA-2 (show PTPRN ELISA Kits) antibodies versus those patients with negative auto-antibodies and GAD65+ auto-antibodies after simultaneous pancreas kidney transplantation.
Plasma GAD65 qualifies as a marker for early beta-cell loss after intraportal transplantation.
Cohort study shows that mean GAD65 mRNA levels in the prefrontal cortex area 9 are not altered in subjects with schizophrenia but are lower in subjects with schizoaffective disorder
Data suggest that women with gestational diabetes who develop autoantibodies against GAD2 (glutamate decarboxylase 2) exhibit higher blood glucose levels, insulin (show INS ELISA Kits) resistance, and impaired insulin (show INS ELISA Kits) secretion from beta cells in the postpartum period.
GABA is the major inhibitory neurotransmitter in the brain. We show that Dlx1/Dlx2 homeobox (show PRRX1 ELISA Kits) genes regulate GABA synthesis during forebrain development through direct activation of glutamic acid decarboxylase (show GAD ELISA Kits) enzyme isoforms that convert glutamate (show GRIN1 ELISA Kits) to GABA.
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.
Increased activity due to bicuculline preferentially up-regulated GAD65. This was reduced by AP5 (show AP5B1 ELISA Kits), a selective blocker of Ca2 (show CA2 ELISA Kits)+-permeable ion channels and NMDA-Rs, and by U0126, KN93, and K252a, affecting BDNF (show BDNF ELISA Kits) pathways.
Data show that miRNAs are involved in regulating the expression of the major type 1 diabetes (T1D) autoantigens IA-2 (show PTPRN ELISA Kits), IA-2beta (show PTPRN2 ELISA Kits), and GAD65 enzyme.
Results indicate the significant contribution of not only GAD65, GAD67 (show GAD1 ELISA Kits) and VGAT (show SLC32A1 ELISA Kits)-mediated GABAergic but also glycinergic transmissions to both palate and abdominal wall formations
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.
Results show that GAD65 is required for efficient GABAergic synaptic transmission and plasticity, and for maintaining extracellular GABA at (show ABAT ELISA Kits) a level needed for associative plasticity at cortical inputs in the lateral amygdala
Menin regulates spinal glutamate (show GRIN1 ELISA Kits)-GABA balance through GAD65 contributing to neuropathic pain.
Our data suggest a role of GAD65-mediated GABA synthesis in the encoding of circadian information to fear memory
Autoimmunity to GAD65 may play a role in the development of Stiff person syndrome.
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. Alternative splicing results in multiple transcript variants that encode the same protein.
glutamate decarboxylase 2 (pancreatic islets and brain, 65kDa)
, glutamate decarboxylase 2
, glutamic acid decarboxylase
, 65 kDa glutamic acid decarboxylase
, Glutamate decarboxylase 2 (islet)
, glutamate decarboxylase 65 kDa isoform
, glutamic acid decarboxylase 2
, glutamic acid decarboxylase 65
, Glutamate decarboxylase-2 (pancreas)