AG252
GAD Peptide
control for AB1511, powder
Sinónimos:
GAD
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About This Item
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product name
GAD, control peptide for AB1511,
biological source
rat
Quality Level
assay
>80%
form
powder
manufacturer/tradename
Chemicon®
technique(s)
cell based assay: suitable
NCBI accession no.
UniProt accession no.
shipped in
dry ice
Gene Information
rat ... GAD2(24380)
General description
Synthetic peptide corresponding to amino acid residues Cys+ 572-585 of rat GAD65 (Erlander et al., 1991). The amino acid sequence is wholly conserved in rat GAD67, and the peptide is located at the C-terminus in both forms of the enzyme. Sequence: [C]DFLIEEIERLGQDL.
Application
Antibody blocking (AB1511)
Optimal working dilution must be determined by the end user.
Optimal working dilution must be determined by the end user.
Research Category
Neuroscience
Neuroscience
Research Sub Category
Neurotransmitters & Receptors
Neuronal & Glial Markers
Neurotransmitters & Receptors
Neuronal & Glial Markers
Physical form
White lyophilized powder. Soluble in water.
Storage and Stability
Long term storage at -20°C in a sealed container with desiccant for up to 12 months after date of receipt.
Legal Information
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
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.
Storage Class
11 - Combustible Solids
wgk_germany
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificados de análisis (COA)
Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»
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Nature communications, 11(1), 869-869 (2020-02-15)
Spinal disinhibition has been hypothesized to underlie pain hypersensitivity in neuropathic pain. Apparently contradictory mechanisms have been reported, raising questions on the best target to produce analgesia. Here, we show that nerve injury is associated with a reduction in the
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