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GAD1 encodes one of several forms of glutamic acid decarboxylase, identified as a major autoantigen in insulin-dependent diabetes. Additionally we are shipping GAD Kits (27) and GAD Proteins (10) and many more products for this protein.
Showing 10 out of 178 products:
Rat (Rattus) Polyclonal GAD Primary Antibody for WB - ABIN1574123
Ketzef, Kahn, Weissberg, Becker, Friedman, Gitler: Compensatory network alterations upon onset of epilepsy in synapsin triple knock-out mice. in Neuroscience 2011
Show all 2 references for ABIN1574123
Human Polyclonal GAD Primary Antibody for ELISA, WB - ABIN334405
Huang, Akbarian: GAD1 mRNA expression and DNA methylation in prefrontal cortex of subjects with schizophrenia. in PLoS ONE 2007
Human Polyclonal GAD Primary Antibody for WB - ABIN655175
Ruaño, Thompson, Kane, Pullinger, Windemuth, Seip, Kocherla, Holford, Wu: Physiogenomic analysis of statin-treated patients: domain-specific counter effects within the ACACB gene on low-density lipoprotein cholesterol? in Pharmacogenomics 2010
Gad1 knockdown mice have pronounced sensorimotor gating deficits, increased novelty-seeking and reduced fear extinction
The neuronal marker UCH-L1 (show UCHL1 Antibodies) is induced in, and specifically augments the oncogene (show RAB1A Antibodies)-induced transformation of, germinal center B cells.
Glutamate decarboxylase (show GLUL Antibodies) expression may be a reliable proxy of altered GABAergic transmission.
Activity deprivation due to TTX preferentially down-regulated GAD67. BDNF (show BDNF Antibodies)-induced increase in the GAD67 protein was markedly lower than that of GAD65 (show GAD2 Antibodies), indicating that BDNF (show BDNF Antibodies) differentially regulates activity-dependent gene expression of the 2 isoforms.
The results of this study indicated that the mice heterozygous for GAD67 deficiency primarily in PV neurons share several neurochemical and behavioral abnormalities with schizophrenia.
Data demonstrate that GAD67 levels directly influence synaptic inhibition.
The GAD65 (show GAD2 Antibodies)-independent mechanism for targeting of GAD67 to synaptic vesicles in neurons is not functional in islet beta-cells.
Pharmacological inhibition of UCHL1 (show UCHL1 Antibodies) exacerbates rather than ameliorates disease symptoms in a mouse model of SMA (show SMN1 Antibodies). Thus, pharmacological inhibition of UCHL1 (show UCHL1 Antibodies) is not a viable therapeutic target for SMA (show SMN1 Antibodies).
Results indicate the significant contribution of not only GAD65 (show GAD2 Antibodies), GAD67 and VGAT (show SLC32A1 Antibodies)-mediated GABAergic but also glycinergic transmissions to both palate and abdominal wall formations
These findings provide original evidence that striatal Gad67 expression is involved in the modulation of learning and social behavior.
mutations in the two lobes affect GAD1 activation in similar ways and only intact AtCaM1 can fully activate GAD1. Taken together, our data provide new insights into the CaM (show CALM Antibodies) lobes role in interactions between CaM (show CALM Antibodies) and plant GAD.
Insertion mutants of GAD1 revealed that GABA levels in roots were drastically reduced compared with those in the wild type.
Calmodulin (show CALM Antibodies) activates Gad1 in a unique way by relieving two C-terminal autoinhibition domains of adjacent active sites, forming a 393 kDa Gad1-calmodulin (show CALM Antibodies) complex with an unusual 1:3 stoichiometry.
This study showed that in female groups, the expression of GABRA5 (show GABRA5 Antibodies) was generally higher in schizophrenia cases compared to the control.
GAD autoantibodies were associated with risk of developing type 1 diabetes.
Conversion of GAD autoantibody is associated with patients with presumed type 2 diabetes.
Gene ransfer of GAD67 by herpes simplex virus vectors prevents HIV gp120 (show ITIH4 Antibodies)/ddC (show DDC Antibodies)-induced neuropathic pain.
Phosphate-activated glutaminase (show GLS2 Antibodies) and GAD65 (show GAD2 Antibodies)/67 concentrations are compared in Alzheimer's disease cerebellum versus normal cerebellum controls
results statistically show that a reduction in GAD1 and SCL1A2 expression in the dorsolateral prefrontal cortex in subjects with major depressive disorder is related to a possible attenuated RAF (show RAF1 Antibodies)/MEK (show MAP2K1 Antibodies)/ERK (show EPHB2 Antibodies) pathway
CNR1 (show CNR1 Antibodies), GAD1 and BDNF (show BDNF Antibodies) polymorphisms are associated with male heroin dependence in the Dai (show ZBP1 Antibodies) population in China.
The decreased amount of GAD65 (show GAD2 Antibodies) and GAD67 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.
Deficient Zif268 (show EGR1 Antibodies) mRNA expression may contribute to lower cortical GAD67 levels in schizophrenia, suggesting altered cortical GABA synthesis and impaired cognition in schizophrenia.
These results suggest that the GAD1 gene is a strong candidate gene that affects growth traits in cattle.
relative expression domains of the dlx and gad1 genes in the zebrafish telencephalon and diencephalon
High levels of GAD67 mRNA were observed in the intermediate and ventral parts of the medial pallium
the distribution of GAD67-expressing cells highly resembles the distribution of gamma-aminobutyric acid (GABA)/GAD67-expressing cells found in the early zebrafish (teleost) forebrain, suggesting a prosomeric fate map of GABAergic cell populations
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. Deficiency in this enzyme has been shown to lead to pyridoxine dependency with seizures. Alternative splicing of this gene results in two products, the predominant 67-kD form and a less-frequent 25-kD form.
glutamate decarboxylase 1
, glutamate decarboxylase 2 (pancreatic islets and brain, 65kDa)
, glutamic acid decarboxylase 65-like protein
, 67 kDa glutamic acid decarboxylase
, GLUTAMATE DECARBOXYLASE, 67 KD ISOFORM (GAD-67) (67 KD GLUTAMIC ACID DECARBOXYLASE)
, glutamate decarboxylase 67 kDa isoform
, glutamic acid decarboxylase 1
, Glutamate decarboxylase 1 (brain)
, glutamate decarboxylase 1 variant GAD67NT
, glutamic acid decarboxylase
, glutamate decarboxylase 67
, glutamate decarboxylase, 67 kDa isoform
, gracile axonal dystrophy
, neuron cytoplasmic protein 9.5
, protein gene product 9.5
, ubiquitin carboxyl-terminal hydrolase isozyme L1
, ubiquitin thioesterase L1