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Key Documents

ABN101

Sigma-Aldrich

Anti-GAD65 Antibody

from rabbit, purified by affinity chromatography

Synonyme(s) :

Glutamate decarboxylase 2, 65 kDa glutamic acid decarboxylase, GAD-65, Glutamate decarboxylase 65 kDa isoform

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About This Item

Code UNSPSC :
12352203
eCl@ss :
32160702
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Niveau de qualité

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Produit purifié par

affinity chromatography

Espèces réactives

mouse, human, rat, pig

Réactivité de l'espèce (prédite par homologie)

canine (based on 100% sequence homology), porcine (based on 100% sequence homology)

Technique(s)

western blot: suitable

Numéro d'accès NCBI

Numéro d'accès UniProt

Conditions d'expédition

wet ice

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... GAD2(2572)

Description générale

GAD65 is a group II decarboxylase enzyme that catalyzes the biosynthesis of GABA from glutamate with the aid of the cofactor, pyridoxal 5′-phosphate. GAD65 localizes at presynaptic GABAergic terminals and is reported to supply local vesicular pools of GABA facilitating transient inhibitiory neurotransmission, although GAD65 may also play a role in more sustained tonic inhibitory signals. It is present as a dimer of alpha and beta subunits and is regulated by alternative splicing, which may produce the GAD67 isoform. GAD65 also undergoes post-translational modifications such as palmitoylation of N-terminal cysteine residues and phosphorylation of multiple alpha-subunit serine residues that enable membrane-anchoring and other vesicular activities. GAD65 has been implicated in neurological conditions resulting from failure of inhibitory neurotransmission such as Huntington′s disease and epilepsy. In addition to its CNS presence, GAD65 also produces GABA in pancreatic beta cells and dysfunction in this area may contribute to the pathogenesis of insulin-dependent diabetes mellitus.

Immunogène

KLH-conjugated linear peptide corresponding to human GAD65.

Application

Anti-GAD Antibody is an antibody against GAD65 for use in Western Blotting. See below for more information about this anti GAD antibody.
Research Category
Neuroscience
Research Sub Category
Developmental Neuroscience
Western Blot Analysis: 1 µg/mL from a representative lot detected GAD65 on 10 µg of rat brain membrane tissue lysate. Western Blot performed without Tween.

Qualité

Evaluated by Western Blot in rat brain membrane tissue lysate.

Western Blot Analysis: 1 µg/mL of this antibody detected GAD65 on 10 µg of rat brain membrane tissue lysate.

Description de la cible

~59/63 kDa observed. The calculated molecular weight is 65 kDa, however GAD65 has been shown as a ~59/63 doublet in western blots. (Christgau, S., et al. (1991). Journal of Biological Chemistry. 266(31):21257-21264.) An uncharacterized band appears at ~38 kDa in some lysates.

Forme physique

Affinity purified
Purified Rabbit Polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Stockage et stabilité

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

Remarque sur l'analyse

Control
Rat brain membrane tissue lysate

Autres remarques

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Clause de non-responsabilité

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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Code de la classe de stockage

12 - Non Combustible Liquids

Classe de danger pour l'eau (WGK)

WGK 1

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.

Consulter la Bibliothèque de documents

Pancreatic beta cells express two autoantigenic forms of glutamic acid decarboxylase, a 65-kDa hydrophilic form and a 64-kDa amphiphilic form which can be both membrane-bound and soluble.
Christgau, S, et al.
The Journal of Biological Chemistry, 266, 21257-21264 (1991)
Dany Arsenault et al.
Biology of sex differences, 11(1), 63-63 (2020-11-18)
While the higher prevalence of Alzheimer's disease (AD) in women is clear, studies suggest that biological sex may also influence AD pathogenesis. However, mechanisms behind these differences are not clear. To investigate physiological differences between sexes at the cellular level in the
Cyril Bories et al.
Aging, 9(5), 1386-1403 (2017-05-20)
Defects in p21-activated kinase (PAK) lead to dendritic spine abnormalities and are sufficient to cause cognition impairment. The decrease in PAK in the brain of Alzheimer's disease (AD) patients is suspected to underlie synaptic and dendritic disturbances associated with its
Margaret Jia et al.
Learning & memory (Cold Spring Harbor, N.Y.), 25(10), 533-543 (2018-09-19)
The medial prefrontal cortex (mPFC) plays a critical role in complex brain functions including decision-making, integration of emotional, and cognitive aspects in memory processing and memory consolidation. Because relatively little is known about the molecular mechanisms underlying its development, we
Masafumi Shimojo et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 40(17), 3491-3501 (2020-04-09)
Synaptic dysfunction provoking dysregulated cortical neural circuits is currently hypothesized as a key pathophysiological process underlying clinical manifestations in Alzheimer's disease and related neurodegenerative tauopathies. Here, we conducted PET along with postmortem assays to investigate time course changes of excitatory

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