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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 (219) and GAD65 Kits (24) and many more products for this protein.
Showing 10 out of 17 products:
Mouse (Murine) GAD65 Protein expressed in Baculovirus infected Insect Cells - ABIN2008111
Swarbrick, Waldenmaier, Pennacchio, Lind, Cavazos, Geller, Merriman, Ustaszewska, Malloy, Scherag, Hsueh, Rief, Mauvais-Jarvis, Pullinger, Kane, Dent, McPherson, Kwok, Hinney, Hebebrand, Vaisse: Lack of support for the association between GAD2 polymorphisms and severe human obesity. in PLoS biology 2005
Show all 2 references for ABIN2008111
Human GAD65 Protein expressed in Wheat germ - ABIN1354671
Grupillo, Gualtierotti, He, Sisino, Bottino, Rudert, Trucco, Fan: Essential roles of insulin expression in Aire+ tolerogenic dendritic cells in maintaining peripheral self-tolerance of islet ?-cells. in Cellular immunology 2012
Show all 2 references for ABIN1354671
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.
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) autoantibody (Ab) levels and single nucleotide polymorphisms (SNPs) of the glutamic acid de-carboxylase 2 (GAD2) 5'-untranslated region
GAD (show GAD1 Proteins) 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 Proteins) 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 Proteins) resistance, and impaired insulin (show INS Proteins) secretion from beta cells in the postpartum period.
Phosphate-activated glutaminase (show GLS2 Proteins) and GAD65/67 concentrations are compared in Alzheimer's disease cerebellum versus normal cerebellum controls
GAD2 SNPs significantly associate with early-onset obsessive compulsive disorder.
The decreased amount of GAD65 and GAD67 (show GAD1 Proteins) suggests the decreased synthesis of neurotransmitter and basic GABA pools that indicates insufficient functioning of the GABA system in the cerebellar cortex of Alzheimer's disease patients.
Increased activity due to bicuculline preferentially up-regulated GAD65. This was reduced by AP5, a selective blocker of Ca2 (show CA2 Proteins)+-permeable ion channels and NMDA-Rs, and by U0126, KN93, and K252a, affecting BDNF (show BDNF Proteins) pathways.
Data show that miRNAs are involved in regulating the expression of the major type 1 diabetes (T1D) autoantigens IA-2 (show PTPRN Proteins), IA-2beta (show PTPRN2 Proteins), and GAD65 enzyme.
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
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 Proteins) a level needed for associative plasticity at cortical inputs in the lateral amygdala
Menin (show MEN1 Proteins) regulates spinal glutamate (show GRIN1 Proteins)-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.
Prenatal and postnatal maternal effects influence GAD65 and GAD67 (show GAD1 Proteins) gene expression depending on the age of the offspring.
These findings indicate novel, differential roles for GluN2A (show GRIN2A Proteins), B and D receptors and for GAD65-mediated GABA in the regulation of individual topographies of orofacial movement
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)