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Glutamic Acid Decarboxylase Protein (GAD)

Protéine Recombinant Glutamic Acid Decarboxylase exprimée dans Escherichia coli (E. coli).
N° du produit ABIN7849740
572,00 €
Plus frais de livraison 40,00 € et TVA
100 μg
Destination: France
Envoi sous 9 à 11 jours ouvrables

Aperçu rapide pour Glutamic Acid Decarboxylase Protein (GAD) (ABIN7849740)

Antigène

Glutamic Acid Decarboxylase (GAD)

Type de proteíne

Recombinant

Origine

Humain

Source

Escherichia coli (E. coli)

Application

ELISA

Pureté

>85 % by SDS-PAGE
  • Fonction

    Recombinant Human Glutamic Acid Decarboxylase230,GAD230 Protein
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  • Indications d'application

    Optimal working dilution should be determined by the investigator.

    Restrictions

    For Research Use only
  • Format

    Liquid

    Buffer

    Tris-HCl, pH 7.4±0.2 with 0.02 % Sodium azide.

    Agent conservateur

    Sodium azide

    Précaution d'utilisation

    This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

    Stock

    4 °C,-20 °C

    Stockage commentaire

    Ship at 4°C. Upon receipt, aliquot and store at -20°C for long term. Avoid repeated freeze and thaw cycles.
  • Antigène

    Glutamic Acid Decarboxylase (GAD)

    Autre désignation

    GAD230

    Sujet

    Synonyms: Glutamic Acid Decarboxylase, Glutamic Acid Decarboxylase 230, GAD230

    Description: Recombinant human Glutamic Acid Decarboxylase 230 protein with molecular weight of 45 kDa.

    Background: Glutamate decarboxylase or glutamic acid decarboxylase (GAD) is an enzyme that catalyzes the decarboxylation of glutamate to GABA and CO2. In mammals, GAD exists in two isoforms encoded by two different genes - GAD1 and GAD2. These isoforms are GAD67 and GAD65 with molecular weights of 67 and 65 kDa, respectively. GAD65 and GAD67 synthesize GABA at different locations in the cell, at different developmental times, and for functionally different purposes. GAD67 is spread evenly throughout the cell while GAD65 is localized to nerve terminals. Gad67 in Drd1a-expressing neurons plays a key role in the development of LID and they support the hypothesis that altered GABAergic neurotransmission in the direct pathway is involved in dyskinesia.

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