G5163
Anti-Glutamic Acid Decarboxylase 65/67 antibody produced in rabbit
IgG fraction of antiserum, buffered aqueous solution
Synonym(s):
Anti-GAD 65/67
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About This Item
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biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
IgG fraction of antiserum
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen 65-67 kDa
species reactivity
rat, mouse, feline, pig, human
packaging
antibody small pack of 25 μL
enhanced validation
independent
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technique(s)
immunohistochemistry (formalin-fixed, paraffin-embedded sections): 1:1,000 using tissue sections of rat pancreas
microarray: suitable
western blot: 1:10,000 using rat brain extract
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... GAD2(2572)
mouse ... Gad2(14417)
rat ... Gad2(24380)
Related Categories
General description
GAD 65 has been identified as an autoantigen in insulin dependent diabetes mellitus (IDDM) and stiff-man syndrome (SMS).
GAD is highly expressed in GABAergic neurons and pancreatic β cells. It is transiently expressed in non-GABAergic embryonic and adult neurons, indicating a role in development. It is also present in testis, oviduct, and ovary GAD exists as two isoforms, GAD 65 and GAD 67 (molecular masses of 65 and 67 kDa, respectively) that are encoded by two different genes. GAD65 is an ampiphilic, membrane anchored protein, (585 amino acid residues) and is encoded on human chromosome 10. GAD 67 is a cytoplasmic protein (594 amino acid residues) and is encoded on chromosome 2. There is 64% amino acid idENTITY_TYPE_CODE. The two isoforms appear to have distinct intraneuronal distribution in the brain. The protein is initially localized to cytosol and then gets anchored to the membrane upon post translational modification. The GAD2 gene is mapped to human chromosome 10p12.1.
Specificity
Reacts specifically with GAD 65 and GAD 67 isoforms from brain.
Reacts specifically with GAD 65 and GAD 67 isoforms in extracts of rat brain and rat pancreas.
Immunogen
synthetic peptide corresponding to the C-terminal region of human GAD 67 (amino acids 579-594). The sequence is identical in human GAD 65 (amino acids 570-585), in rat, mouse, and pig GAD 65, in rat, pig, and cat GAD 67, and is highly conserved in GAD 67 of mouse origin (single amino acid substitution).
Application
Anti-GAD 65/67 may be used for the detection and localization of GAD 65/67 isoforms by immunofluorescence and immunohistochemistry in rat retinal cells, human subthalamus neurons, and pancreatic β-cells of rat. The minimum working dilution that may be used is 1:10000. Detection by immunoblotting may be possible in brain cells of monkey, human, rat and gecko. at a minimum working dilution of 1:1000.
Anti-Glutamic Acid Decarboxylase 65/67 antibody produced in rabbit has also been used in Immunohistochemistry and Immunocytochemistry.
Biochem/physiol Actions
Glutamic acid decarboxylase (GAD) is the key enzyme that catalyses the conversion of L-glutamate to γ-aminobutyric acid (GABA). GABA is a principal inhibitory neurotransmitter and a paracrine signal molecule in pancreatic islet cells. GAD 65 has been identified as an autoantigen in insulin dependent diabetes mellitus (IDDM) and stiff-man syndrome (SMS).
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
Disclaimer
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.
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Storage Class
10 - Combustible liquids
wgk_germany
WGK 2
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificates of Analysis (COA)
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John A Gebe et al.
Journal of autoimmunity, 30(4), 197-206 (2007-10-24)
A human T-cell receptor (TcR) derived from an autoreactive T-cell specific for GAD65, from a subject at high risk for autoimmune diabetes, was introduced into HLA-DR4 transgenic mice. The source of TcR was a CD4(+) T(H)1(+) T-cell clone which responded
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Phelps E A, et al.
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Podrygajlo G, et al.
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Transgenic rats expressing enhanced green fluorescent protein (EGFP) under the control of an estrogen receptor (ER) alpha promoter were generated to tag ERalpha-positive neurons in the brain. Two transgenes, one containing sequences for promoter A and DsRed and the other
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