MAB5406 Anti-GAD67 Antibody, clone 1G10.2

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      Replacement Information

      Key Specifications Table

      Species ReactivityKey ApplicationsHostFormatAntibody Type
      H, R, M IHC, IH(P), WB M Purified Monoclonal Antibody
      Catalogue NumberMAB5406
      ReplacesAB5992; AB5862P
      Brand Family Chemicon®
      Trade Name
      • Chemicon
      DescriptionAnti-GAD67 Antibody, clone 1G10.2
      Alternate Names
      • Glutamate Decarboxylase 67kDa Isoform
      • Glutamate Decarboxylase 1
      • Glutamic acid decarboxylase 1
      Background InformationGutamic acid decarboxylase (GAD; E.C. is the enzyme responsible for the conversion of glutamic acid to gamma-aminobutyric acid (GABA), the major inhibitory transmitter in higher brain regions, and putative paracrine hormone in pancreatic islets. Two molecular forms of GAD (65 kDa and 67 kDa, 64% aa identity between forms) are highly conserved and both forms are expressed in the CNS, pancreatic islet cells, testis, oviduct and ovary. The isoforms are regionally distributed cytoplasmically in the brains of rats and mice (Sheikh, 1999). GAD65 is an amphiphilic, membrane-anchored protein (585 a.a.), encoded on human chromosome 10, and is responsible for vesicular GABA production. GAD67 is cytoplasmic (594 a.a.), encoded on chromosome 2, and seems to be responsible for significant cytoplasmic GABA production. GAD expression changes during neural development in rat spinal cord. GAD65 is expressed transiently in commissural axons around E13 but is down regulated the next day while GAD67 expression increases mostly in the somata of those neurons (Phelps, 1999). In mature rat pancreas, GAD65 and GAD67 appear to be differentially localized, GAD65 primarily in insulin-containing beta cells and GAD67 in glucagon-containing (A) cells (Li, 1995). GAD67 expression seems to be particularly plastic and can change in response to experimental manipulation (for example neuronal stimulation or transection) or disease progression and emergent disorders like schizophrenia (Volk, 2000). Colocalization of the two GAD isoforms also shows changes in GAD65/GAD67 distributions correlated with certain disease states such as IDDM and SMS.
      Product Information
      • SKNSH cell lysate (human neuroblastoma), mouse cerebral cortex.
      PresentationPurified mouse monoclonal IgG2a in buffer containing 0.1% sodium azide
      Quality LevelMQ100
      ApplicationThis Anti-GAD Antibody, clone 1G10.2 is validated for use in IH, IH(P), WB for the detection of GAD67. This Anti GAD antibody has more than 75 product citations.
      Key Applications
      • Immunohistochemistry
      • Immunohistochemistry (Paraffin)
      • Western Blotting
      Application NotesWestern Blot: A 1:5,000-1:10,000 dilution was used on a previous lot using ECL on rat and mouse brain lysate.

      Immunohistochemistry on 4% paraformaldehyde fixed mouse and rat tissue: 1:1,000-1:5,000. The antibody has also worked well on human tissue fixed for 10 minutes in 4% PFA at 4°C or 100% ethanol at +20°C or 100% acetone at -20°C at dilutions of 1:2,500-1:5,000.
      A polyclonal to GAD67 is also available as AB5992.

      Optimal working dilutions must be determined by end user.
      Biological Information
      ImmunogenRecombinant GAD67 protein
      ConcentrationPlease refer to the Certificate of Analysis for the lot-specific concentration.
      SpecificityReacts with the 67kDa isoform of Glutamate Decarboxylase (GAD67) of rat, mouse and human origins, other species not yet tested. No detectable cross reactivity with GAD65 by Western blot on rat brain lysate when compared to blot probed with AB1511 that reacts with both GAD65 & GAD67.
      Species Reactivity
      • Human
      • Rat
      • Mouse
      Antibody TypeMonoclonal Antibody
      Entrez Gene Number
      Entrez Gene SummaryThis 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.
      Gene Symbol
      • GAD1
      • SCP
      • GAD-67
      • FLJ45882
      • GAD67
      • GAD
      • EC
      Purification MethodProtein A Purfied
      UniProt Number
      UniProt SummaryFUNCTION: SwissProt: Q99259 # Catalyzes the production of GABA.
      COFACTOR: Pyridoxal phosphate.
      SIZE: 594 amino acids; 66897 Da
      SUBUNIT: Homodimer.
      TISSUE SPECIFICITY: GAD67 is expressed in the CNS, pancreatic islet cells, testis, oviduct and ovary.
      DISEASE: SwissProt: Q99259 # Defects in GAD1 are the cause of autosomal recessive symmetric spastic cerebral palsy (SCP) [MIM:603513]. Cerebral palsy (CP) is an heterogeneous group of neurological disorders of movement and/or posture, with an estimated incidence of 1 in 250 to 1'000 live births, making CP one the commonest congenital disabilities. Non-progressive forms of symmetrical, spastic CP have been identified, which show a Mendelian autosomal recessive pattern of inheritance. Patients present developmental delay, mental retardation and sometimes epilepsy as part of the phenotype.
      SIMILARITY: SwissProt: Q99259 ## Belongs to the group II decarboxylase family.
      Molecular Weight67 kDa
      Physicochemical Information
      Materials Information
      Toxicological Information
      Safety Information according to GHS
      Safety Information
      Product Usage Statements
      Quality AssuranceRoutinely evaluated by immunohistochemistry by SKNSH cell lysate.

      Immunohistochemistry(paraffin) Analysis:
      Representative staining pattern and morphology of GAD67 in somatosensory 1, barrel field of the mouse cerebral cortex. All brown spots are Lamina VI a neurons. No Epitope retrieval was necessary. This lot of the antibody was diluted to 1:500, using IHC Select® Detection with HRP-DAB.
      Optimal Staining pattern/morphology of GAD67: Mouse Brain.
      Usage Statement
      • Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
      Storage and Shipping Information
      Storage ConditionsStable for 6 months at 2-8ºC in undiluted aliquots from date of receipt.
      Packaging Information
      Material Size100 µg
      Transport Information
      Supplemental Information


      Anti-GAD67 Antibody, clone 1G10.2 SDS


      Safety Data Sheet (SDS) 

      Anti-GAD67 Antibody, clone 1G10.2 Certificates of Analysis

      TitleLot Number
      Anti-GAD67, clone 1G10.22464596
      Anti-GAD67, clone 1G10.2 - 23103592310359
      Anti-GAD67, clone 1G10.2 - 23905252390525
      Anti-GAD67, clone 1G10.2 - 19764051976405
      Anti-GAD67, clone 1G10.2 - 20427872042787
      Anti-GAD67, clone 1G10.2 - 20904502090450
      Anti-GAD67, clone 1G10.2 - 21884942188494
      Anti-GAD67, clone 1G10.2 - 22833382283338
      Anti-GAD67, clone 1G10.2 - 31707993170799
      Anti-GAD67, clone 1G10.2 - 32164883216488


      Reference overviewApplicationSpeciesPub Med ID
      An anterograde rabies virus vector for high-resolution large-scale reconstruction of 3D neuron morphology.
      Haberl, MG; Viana da Silva, S; Guest, JM; Ginger, M; Ghanem, A; Mulle, C; Oberlaender, M; Conzelmann, KK; Frick, A
      Brain structure & function  220  1369-79  2015

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      Altered activity of the medial prefrontal cortex and amygdala during acquisition and extinction of an active avoidance task.
      Jiao, X; Beck, KD; Myers, CE; Servatius, RJ; Pang, KC
      Frontiers in behavioral neuroscience  9  249  2015

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      Neuronal BDNF signaling is necessary for the effects of treadmill exercise on synaptic stripping of axotomized motoneurons.
      Krakowiak, J; Liu, C; Papudesu, C; Ward, PJ; Wilhelm, JC; English, AW
      Neural plasticity  2015  392591  2015

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      A retrograde adeno-associated virus for collecting ribosome-bound mRNA from anatomically defined projection neurons.
      Cook-Snyder, DR; Jones, A; Reijmers, LG
      Frontiers in molecular neuroscience  8  56  2015

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      Tfap2a and 2b act downstream of Ptf1a to promote amacrine cell differentiation during retinogenesis.
      Jin, K; Jiang, H; Xiao, D; Zou, M; Zhu, J; Xiang, M
      Molecular brain  8  28  2015

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      Glucocorticoid receptors in the locus coeruleus mediate sleep disorders caused by repeated corticosterone treatment.
      Wang, ZJ; Zhang, XQ; Cui, XY; Cui, SY; Yu, B; Sheng, ZF; Li, SJ; Cao, Q; Huang, YL; Xu, YP; Zhang, YH
      Scientific reports  5  9442  2015

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      TWIK-Related Spinal Cord K⁺ Channel Expression Is Increased in the Spinal Dorsal Horn after Spinal Nerve Ligation.
      Hwang, HY; Zhang, E; Park, S; Chung, W; Lee, S; Kim, DW; Ko, Y; Lee, W
      Yonsei medical journal  56  1307-15  2015

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      A Novel 1,4-Dihydropyridine Derivative Improves Spatial Learning and Memory and Modifies Brain Protein Expression in Wild Type and Transgenic APPSweDI Mice.
      Jansone, B; Kadish, I; van Groen, T; Beitnere, U; Moore, DR; Plotniece, A; Pajuste, K; Klusa, V
      PloS one  10  e0127686  2015

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      Localization of reelin signaling pathway components in murine midbrain and striatum.
      Sharaf, A; Rahhal, B; Spittau, B; Roussa, E
      Cell and tissue research  359  393-407  2015

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      Forebrain deletion of the dystonia protein torsinA causes dystonic-like movements and loss of striatal cholinergic neurons.
      Pappas, SS; Darr, K; Holley, SM; Cepeda, C; Mabrouk, OS; Wong, JM; LeWitt, TM; Paudel, R; Houlden, H; Kennedy, RT; Levine, MS; Dauer, WT
      eLife  4  e08352  2015

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