anti-Glutamate Decarboxylase 2 (Pancreatic Islets and Brain, 65kDa) (GAD2) Antibodies

Rhesus Monkey Glutamate Decarboxylase 2 (Pancreatic Islets and Brain, 65kDa) (GAD2) interaction partners

1. Results describe the gross distribution patterns of GAD65 in human and rhesus monkey thalami and show that they are nearly identical.

Zebrafish Glutamate Decarboxylase 2 (Pancreatic Islets and Brain, 65kDa) (GAD2) interaction partners

1. GAD65 mRNA was found in the periaqueductal gray.

Human Glutamate Decarboxylase 2 (Pancreatic Islets and Brain, 65kDa) (GAD2) interaction partners

1. healthy donor NK cells showed similar degranulation against both GAD65 AA 114-122 pulsed and unpulsed APCs (show APCS Antibodies). The pathogenetic significance of the CD3 (show CD3 Antibodies)-CD8dullCD56+ 'memory-like NK cell subset' with increased response upon secondary challenge in diabetics remains to be elucidated

2. Genetic variability in GAD2 and GAD1 (show GAD1 Antibodies) contributes to risk of methamphetamine dependence in the Thai population.

3. 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.

4. 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.

5. 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

6. GAD (show GAD1 Antibodies) autoantibodies were associated with risk of developing type 1 diabetes.

7. Kaplan-Meier survival curves estimated a worst pancreas graft survival for patients with positive IA-2 (show PTPRN Antibodies) antibodies versus those patients with negative auto-antibodies and GAD65+ auto-antibodies after simultaneous pancreas kidney transplantation.

8. Plasma GAD65 qualifies as a marker for early beta-cell loss after intraportal transplantation.

9. 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

10. Data suggest that women with gestational diabetes who develop autoantibodies against GAD2 (glutamate decarboxylase 2) exhibit higher blood glucose levels, insulin (show INS Antibodies) resistance, and impaired insulin (show INS Antibodies) secretion from beta cells in the postpartum period.

Mouse (Murine) Glutamate Decarboxylase 2 (Pancreatic Islets and Brain, 65kDa) (GAD2) interaction partners

1. Results suggest age-dependent decrease of GAD65/67 mRNAs but normal densities of certain GABAergic interneurons in the Shank3 (show SHANK3 Antibodies) transgenic mice.

2. GABA is the major inhibitory neurotransmitter in the brain. We show that Dlx1/Dlx2 homeobox (show PRRX1 Antibodies) genes regulate GABA synthesis during forebrain development through direct activation of glutamic acid decarboxylase enzyme isoforms that convert glutamate (show GRIN1 Antibodies) to GABA.

3. 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.

4. Increased activity due to bicuculline preferentially up-regulated GAD65. This was reduced by AP5, a selective blocker of Ca2 (show CA2 Antibodies)+-permeable ion channels and NMDA-Rs, and by U0126, KN93, and K252a, affecting BDNF (show BDNF Antibodies) pathways.

5. Data show that miRNAs are involved in regulating the expression of the major type 1 diabetes (T1D) autoantigens IA-2 (show PTPRN Antibodies), IA-2beta (show PTPRN2 Antibodies), and GAD65 enzyme.

6. Results indicate the significant contribution of not only GAD65, GAD67 (show GAD1 Antibodies) and VGAT (show SLC32A1 Antibodies)-mediated GABAergic but also glycinergic transmissions to both palate and abdominal wall formations

7. 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.

8. Results show that GAD65 is required for efficient GABAergic synaptic transmission and plasticity, and for maintaining extracellular GABA at (show ABAT Antibodies) a level needed for associative plasticity at cortical inputs in the lateral amygdala

9. Menin regulates spinal glutamate (show GRIN1 Antibodies)-GABA balance through GAD65 contributing to neuropathic pain.

10. Our data suggest a role of GAD65-mediated GABA synthesis in the encoding of circadian information to fear memory