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Merck
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ABN904

Sigma-Aldrich

Anti-GAD1/GAD2 Antibody

rabbit polyclonal

Szinonimák:

Glutamate decarboxylase 2/Glutamate decarboxylase 1, 65 kDa/67kDa glutamic acid decarboxylase, GAD-65/67, Glutamate decarboxylase 65/67 kDa isoform

Bejelentkezésa Szervezeti és Szerződéses árazás megtekintéséhez


About This Item

UNSPSC kód:
12352203
eCl@ss:
32160702
NACRES:
NA.41
klón:
polyclonal
application:
IHC
WB
faj reaktivitás:
rat, mouse, human
technika/technikák:
immunohistochemistry: suitable (paraffin)
western blot: suitable
citations:
34

Terméknév

Anti-GAD 65/67, from rabbit, purified by affinity chromatography

biológiai forrás

rabbit

Minőségi szint

antitest forma

affinity isolated antibody

antitest terméktípus

primary antibodies

klón

polyclonal

tisztítva

affinity chromatography

faj reaktivitás

rat, mouse, human

kiszerelés

antibody small pack of 25 μg

technika/technikák

immunohistochemistry: suitable (paraffin)
western blot: suitable

izotípus

IgG

NCBI elérési szám

UniProt elérési szám

kiszállítva

ambient

célzott transzláció utáni módosítás

unmodified

Géninformáció

Általános leírás

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.

Egyediség

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.

Immunogén

Epitope: C-terminus
KLH-conjugated linear peptide corresponding to 14 amino acids from the C-terminal region of human glutamate decarboxylase 2 (GAD2).

Alkalmazás

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

Minőség

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.

Cél megnevezése

~60/62kDa observed; 65.41/66.90 kDa calculated, respectively for GAD2 and GAD1. Uncharacterized bands may be observed in some lysate(s).

Fizikai forma

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.

Tárolás és stabilitás

Stable for 1 year at 2-8°C from date of receipt.

Egyéb megjegyzések

Concentration: Please refer to lot specific datasheet.

Jogi nyilatkozat

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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Tárolási osztály kódja

12 - Non Combustible Liquids

WGK

WGK 1

Lobbanási pont (F)

does not flash

Lobbanási pont (C)

does not flash


Analitikai tanúsítványok (COA)

Analitikai tanúsítványok (COA) keresése a termék sarzs-/tételszámának megadásával. A sarzs- és tételszámok a termék címkéjén találhatók, a „Lot” vagy „Batch” szavak után.

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Az Ön által nemrégiben megvásárolt termékekre vonatkozó dokumentumokat a Dokumentumtárban találja.

Dokumentumtár megtekintése

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).
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
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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