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GAD1 Antibody (C-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, E |
|---|---|
| Primary Accession | Q99259 |
| Other Accession | NP_000808 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 66897 Da |
| Antigen Region | 514-543 aa |
| Gene ID | 2571 |
|---|---|
| Other Names | Glutamate decarboxylase 1, 67 kDa glutamic acid decarboxylase, GAD-67, Glutamate decarboxylase 67 kDa isoform, GAD1, GAD, GAD67 |
| Target/Specificity | This GAD1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 514-543 amino acids from the C-terminal region of human GAD1. |
| Dilution | WB~~1:1000 |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | GAD1 Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | GAD1 (HGNC:4092) |
|---|---|
| Synonyms | GAD, GAD67 |
| Function | Catalyzes the synthesis of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) with pyridoxal 5'-phosphate as cofactor. |
| Tissue Location | [Isoform 1]: Expressed in brain. |
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Provided below are standard protocols that you may find useful for product applications.
Background
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.
References
Lanoue, A.C., et al. Exp. Neurol. 226(1):207-217(2010)
Jia, P., et al. Schizophr. Res. 122 (1-3), 38-42 (2010) :
Terranova, C., et al. Alcohol 44(5):407-413(2010)
Ruano, G., et al. Pharmacogenomics 11(7):959-971(2010)
Jugessur, A., et al. PLoS ONE 5 (7), E11493 (2010) :
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