Recombinant Human GAD1/GAD67 Protein Catalog Number: ATGP2642

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Recombinant human GAD1/GAD67 protein Catalog Number: ATGP2642 PRODUCT INPORMATION Expression system E.coli Domain 1-224aa UniProt No. Q99259 NCBI Accession No. NP_038473 Alternative Names Glutamate decarboxylase 1 isoform GAD25, Glutamate decarboxylase 1 (brain, 67kDa), CPSQ1, GAD, SCP PRODUCT SPECIFICATION Molecular Weight 27.7 kDa (247aa) Concentration 0.5mg/ml (determined by Bradford assay) Formulation Liquid in. 20mM Tris-HCl buffer (pH 8.0) containing 10% glycerol, 0.4M urea Purity > 85% by SDS-PAGE Tag His-Tag Application SDS-PAGE,Denatured Storage Condition Can be stored at +2C to +8C for 1 week. For long term storage, aliquot and store at -20C to -80C. Avoid repeated freezing and thawing cycles. BACKGROUND Description GAD1 is one of several forms of glutamic acid decarboxylase, identified as a major autoantigen in insulin- dependent diabetes. It 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 protien 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- 1 Recombinant human GAD1/GAD67 protein Catalog Number: ATGP2642 frequent 25-kD form. Recombinant human GAD1 protein, fused to His-tag at N-terminus, was expressed in E. coli. Amino acid Sequence MGSSHHHHHH SSGLVPRGSH MGSMASSTPS SSATSSNAGA DPNTTNLRPT TYDTWCGVAH GCTRKLGLKI CGFLQRTNSL EEKSRLVSAF KERQSSKNLL SCENSDRDAR FRRTETDFSN LFARDLLPAK NGEEQTVQFL LEVVDILLNY VRKTFDRSTK VLDFHHPHQL LEGMEGFNLE LSDHPESLEQ ILVDCRDTLK YGVRTGHPRF FNQLSTGLDI IGLAGEWLTS TANTNMPSDM RECWLLR General References Chessler S.D., Lernmark A., et al. (2000) J. Biol. Chem. 275:5188-5192. DATA SDS-PAGE 3ug by SDS-PAGE under reducing condition and visualized by coomassie blue stain. 2.

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Genetic Modulation of GABA Levels in the Anterior Cingulate Cortex by GAD1 and COMT
Neuropsychopharmacology (2010) 35, 1708–1717 & 2010 Nature Publishing Group All rights reserved 0893-133X/10 $32.00 www.neuropsychopharmacology.org Genetic Modulation of GABA Levels in the Anterior Cingulate Cortex by GAD1 and COMT 1,2 1,2 3 1,2 Stefano Marenco* , Antonina A Savostyanova , Jan Willem van der Veen , Matthew Geramita , 1,2 1,2 1 1,2 1 Alexa Stern , Alan S Barnett , Bhaskar Kolachana , Eugenia Radulescu , Fengyu Zhang , 1 1 3 1 Joseph H Callicott , Richard E Straub , Jun Shen and Daniel R Weinberger 1 2 Clinical Brain Disorders Branch, GCAP, IRP, NIMH, Bethesda, MD, USA; Unit for Multimodal Imaging Genetics, Clinical Brain Disorders Branch, 3 GCAP, IRP, NIMH, Bethesda, MD, USA; Magnetic Resonance Spectroscopy Unit, MAP, IRP, NIMH, Bethesda, MD, USA g-Aminobutyric acid (GABA)-ergic transmission is critical for normal cortical function and is likely abnormal in a variety of neuropsychiatric disorders. We tested the in vivo effects of variations in two genes implicated in GABA function on GABA concentrations in prefrontal cortex of living subjects: glutamic acid decarboxylase 1 (GAD1), which encodes GAD67, and catechol-o-methyltransferase (COMT), which regulates synaptic dopamine in the cortex. We studied six single nucleotide polymorphisms (SNPs) in GAD1 previously associated with risk for schizophrenia or cognitive dysfunction and the val158met polymorphism in COMT in 116 healthy volunteers using proton magnetic resonance spectroscopy. Two of the GAD1 SNPs (rs1978340 (p ¼ 0.005) and rs769390 (p ¼ 0.004)) showed effects on GABA levels as did COMT val158met (p ¼ 0.04). We then tested three SNPs in GAD1 (rs1978340, rs11542313, and rs769390) for interaction with COMT val158met based on previous clinical results.
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