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Glutamic Acid Decarboxylase Protein (GAD)

Recombinant Glutamic Acid Decarboxylase protein expressed in Escherichia coli (E. coli).
Catalog No. ABIN7849740
$554.40
Plus shipping costs $50.00
100 μg
Shipping to: United States
Delivery in 11 to 13 Business Days

Quick Overview for Glutamic Acid Decarboxylase Protein (GAD) (ABIN7849740)

Target

Glutamic Acid Decarboxylase (GAD)

Protein Type

Recombinant

Origin

Human

Source

Escherichia coli (E. coli)

Application

ELISA

Purity

>85 % by SDS-PAGE
  • Purpose

    Recombinant Human Glutamic Acid Decarboxylase230,GAD230 Protein
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  • Application Notes

    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.

    Preservative

    Sodium azide

    Precaution of Use

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

    Storage

    4 °C,-20 °C

    Storage Comment

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

    Glutamic Acid Decarboxylase (GAD)

    Alternative Name

    GAD230

    Background

    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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