gamma-aminobutyric Acid (GABA) A Receptor, alpha 4 (GABRA4) (N-Term) Peptide
GABRA4
Reactivité: Humain
Hôte: Synthetic
BP, WB
N° du produit ABIN977207
Aperçu rapide pour gamma-aminobutyric Acid (GABA) A Receptor, alpha 4 (GABRA4) (N-Term) Peptide (ABIN977207)
Antigène
GABRA4
(gamma-aminobutyric Acid (GABA) A Receptor, alpha 4 (GABRA4))
Origine
Humain
Source
Synthetic
Application
Blocking Peptide (BP), Western Blotting (WB)
Protein Region
N-Term
Attributs du produit
This is a synthetic peptide designed for use in combination with anti-GABRA4 antibody (Catalog #: ARP34982_P050). It may block above mentioned antibody from binding to its target protein in western blot and/or immunohistochecmistry under proper experimental settings. There is no guarantee for its use in other applications.
Each Investigator should determine their own optimal working dilution for specific applications.
Restrictions
For Research Use only
Format
Lyophilized
Reconstitution
Add 100 μL of sterile PBS. Final peptide concentration is 1 mg/mL in PBS.
Concentration
1 mg/mL
Buffer
Final peptide concentration is 1 mg/mL in PBS.
Conseil sur la manipulation
Avoid repeated freeze-thaw cycles.
Stock
-20 °C
Stockage commentaire
For longer periods of storage, store at -20°C. Avoid repeat freeze-thaw cycles.
Antigène
GABRA4
(gamma-aminobutyric Acid (GABA) A Receptor, alpha 4 (GABRA4))
Sujet
GABA, the major inhibitory neurotransmitter in the vertebrate brain, mediates neuronal inhibition by binding to the GABA/benzodiazepine receptor and opening an integral chloride channel.GABA is the major inhibitory neurotransmitter in the mammalian brain where it acts at GABA-A receptors, which are ligand-gated chloride channels. Chloride conductance of these channels can be modulated by agents such as benzodiazepines that bind to the GABA-A receptor. At least 16 distinct subunits of GABA-A receptors have been identified. Publication Note: This RefSeq record includes a subset of the publications that are available for this gene. Please see the Entrez Gene record to access additional publications.