ABN904
Anti-GAD 65/67
from rabbit, purified by affinity chromatography
Synonyma:
Glutamate decarboxylase 2/Glutamate decarboxylase 1, 65 kDa/67kDa glutamic acid decarboxylase, GAD-65/67, Glutamate decarboxylase 65/67 kDa isoform
Přihlásitk zobrazení cen stanovených pro organizaci a smluvních cen
About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Doporučené produkty
biological source
rabbit
Quality Level
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
purified by
affinity chromatography
species reactivity
rat, mouse, human
packaging
antibody small pack of 25 μg
technique(s)
immunohistochemistry: suitable (paraffin)
western blot: suitable
isotype
IgG
NCBI accession no.
shipped in
ambient
target post-translational modification
unmodified
Gene Information
human ... GAD1(2571) , GAD2(2572)
General description
Glutamate decarboxylase 2/Glutamate decarboxylase 1 (UniProt: Q05329/Q99259; also known as 65 kDa/67kDa glutamic acid decarboxylase, GAD-65/67, Glutamate decarboxylase 65/67 kDa isoform) is encoded by GAD2/GAD1 (also known as GAD65/GAD67) gene (Gene ID: 2572/2571) in human. Glutamate decarboxylase isoforms are expressed in the brain where it is involved in gamma-aminobutyric acid (GABA) synthesis. Glutamate decarboxylase 2 is also expressed in pancreatic tissue. Both GAD65 and GAD67 synthesize GABA at different locations in the cell and at different developmental stages. Usually, GAD1 is distributed evenly throughout the cell while isoform GAD2 is mainly localized to nerve terminals. GAD1 synthesizes GABA for neuronal activity that is related to as synaptogenesis and protection from neural injury. However, GAD2 isoform synthesizes GABA for neurotransmission activity.
Specificity
This rabbit polyclonal antibody detects GAD2 and GAD1 in human, Mouse, and Rat. It targets an epitope within 14 amino acids from the C-terminal region.
Immunogen
Epitope: C-terminus
KLH-conjugated linear peptide corresponding to 14 amino acids from the C-terminal region of human glutamate decarboxylase 2 (GAD2).
Application
Anti-GAD 65/67 Antibody, Cat. No. ABN904, is a highly specific rabbit polyclonal antibody that targets Human, Mouse, and Rat GAD2 and GAD1 and has been tested in Immunohistochemistry (Paraffin) and Western Blotting.
Immunohistochemistry Analysis: A 1:1,000 dilution from a representative lot detected GAD 65/67 in human cerebellum, mouse cerebral cortex, and rat cerebral cortex tissues.
Research Category
Neuroscience
Neuroscience
Quality
Evaluated by Western Blotting in human brain tissue lysate.
Western Blotting Analysis: 2 µg/mL of this antibody detected GAD 65/67 in 10 µg of human brain tissue lysate.
Western Blotting Analysis: 2 µg/mL of this antibody detected GAD 65/67 in 10 µg of human brain tissue lysate.
Target description
~60/62kDa observed; 65.41/66.90 kDa calculated, respectively for GAD2 and GAD1. Uncharacterized bands may be observed in some lysate(s).
Physical form
Affinity Purified
Purified rabbit polyclonal antibody in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
Storage and Stability
Stable for 1 year at 2-8°C from date of receipt.
Other Notes
Concentration: Please refer to lot specific datasheet.
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
12 - Non Combustible Liquids
wgk_germany
WGK 1
flash_point_f
does not flash
flash_point_c
does not flash
Osvědčení o analýze (COA)
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Již tento produkt vlastníte?
Dokumenty související s produkty, které jste v minulosti zakoupili, byly za účelem usnadnění shromážděny ve vaší Knihovně dokumentů.
Md Main Uddin et al.
ASN neuro, 13, 17590914211035020-17590914211035020 (2021-10-02)
Brain glycogen is remodeled during metabolic homeostasis and provides oxidizable L-lactate equivalents. Brain glycogen phosphorylase (GP)-brain (GPbb; AMP-sensitive) and -muscle (GPmm; norepinephrine-sensitive) type isoforms facilitate stimulus-specific control of glycogen disassembly. Here, a whole animal model involving stereotactic-targeted delivery of GPmm
K P Briski et al.
Brain structure & function, 226(4), 1053-1065 (2021-02-14)
Recurring insulin-induced hypoglycemia (RIIH) in males correlates with maladaptive glucose counter-regulatory collapse and acclimated expression of ventromedial hypothalamic nucleus (VMN) nitric oxide (NO) and γ-aminobutyric acid (GABA) metabolic transmitter biomarkers, e.g., neuronal nitric oxide synthase (nNOS) and glutamate decarboxylase65/67 (GAD).
Khaggeswar Bheemanapally et al.
Scientific reports, 11(1), 16079-16079 (2021-08-11)
Astrocyte glycogen, the primary energy reserve in brain, undergoes continuous remodeling by glucose passage through the glycogen shunt prior to conversion to the oxidizable energy fuel L-lactate. Glucogenic amino acids (GAAs) are a potential non-glucose energy source during neuro-metabolic instability.
Karen P Briski et al.
Acta neurobiologiae experimentalis, 80(1), 57-65 (2020-03-28)
The catecholamine norepinephrine (NE) links hindbrain metabolic‑sensory neurons with downstream gluco‑regulatory loci, including the ventromedial hypothalamic nucleus (VMN). Exogenous NE up‑regulates VMN expression of glutamate decarboxylase (GAD), biomarker for the gluco‑inhibitory transmitter γ‑aminobutryic acid (GABA). Brain glycogen phosphorylase (GP)‑muscle (GPmm)
Abdulrahman Alhamyani et al.
AIMS neuroscience, 8(4), 510-525 (2021-12-09)
Gamma-aminobutyric acid (GABA) acts on ventromedial hypothalamic targets to suppress counter-regulatory hormone release, thereby lowering blood glucose. Maladaptive up-regulation of GABA signaling is implicated in impaired counter-regulatory outflow during recurring insulin-induced hypoglycemia (RIIH). Ventromedial hypothalamic nucleus (VMN) GABAergic neurons express
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