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Anti-GABAA Receptor δ, N-Terminus Antibody
Our Anti-GABAA Receptor δ, N-Terminus primary antibody from PhosphoSolutions is rabbit polyclonal. I
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- BACKGROUND
Application 
| WB, IHC |
|---|---|
| Primary Accession | P18506 |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | IgG |
| Calculated MW | 50566 Da |
| Gene ID | 29689 |
|---|---|
| Other Names | GABA(A) receptor subunit delta antibody, Gabrd antibody, Gamma aminobutyric acid GABA A receptor delta antibody, Gamma aminobutyric acid receptor delta subunit precursor GABA A receptor antibody, Gamma-aminobutyric acid receptor subunit delta antibody, GBRD_HUMAN antibody, MGC45284 antibody |
| Target/Specificity | Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the central nervous system, causing a hyperpolarization of the membrane through the opening of a Cl– channel associated with the GABA-A receptor (GABA-A-R) subtype. GABA-A-Rs are important therapeutic targets for a range of sedative, anxiolytic, and hypnotic agents and are implicated in several diseases including epilepsy, anxiety, depression and substance abuse. The GABA-A-R is a multimeric subunit complex. To date six αs, four βs and four γs, plus alternative splicing variants of some of these subunits, have been identified (Olsen and Tobin,1990; Whiting et al., 1999; Ogris et al., 2004). Injection in oocytes or mammalian cell lines of cRNA coding for α- and β-subunits results in the expression of functional GABA-A-Rs sensitive to GABA. However, co-expression of a γ-subunit is required for benzodiazepine modulation. The various effects of the benzodiazepines in brain may also be mediated via different a-subunits of the receptor (McKernan et al., 2000; Mehta and Ticku, 1998; Ogris et al., 2004; Pöltl et al., 2003). More recently there have been a number of studies demonstrating that the δ-subunit of the receptor may affect subunit assembly (Korpi et al., 2002) and may also confer differential sensitivity to neurosteroids and to ethanol (Wallner et al., 2003; Wohlfarth et al., 2002). |
| Format | Antigen Affinity Purified from Pooled Serum |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | Anti-GABAA Receptor δ, N-Terminus Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Shipping | Blue Ice |
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Provided below are standard protocols that you may find useful for product applications.
Background
Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the central nervous system, causing a hyperpolarization of the membrane through the opening of a Cl– channel associated with the GABA-A receptor (GABA-A-R) subtype. GABA-A-Rs are important therapeutic targets for a range of sedative, anxiolytic, and hypnotic agents and are implicated in several diseases including epilepsy, anxiety, depression and substance abuse. The GABA-A-R is a multimeric subunit complex. To date six αs, four βs and four γs, plus alternative splicing variants of some of these subunits, have been identified (Olsen and Tobin,1990; Whiting et al., 1999; Ogris et al., 2004). Injection in oocytes or mammalian cell lines of cRNA coding for α- and β-subunits results in the expression of functional GABA-A-Rs sensitive to GABA. However, co-expression of a γ-subunit is required for benzodiazepine modulation. The various effects of the benzodiazepines in brain may also be mediated via different a-subunits of the receptor (McKernan et al., 2000; Mehta and Ticku, 1998; Ogris et al., 2004; Pöltl et al., 2003). More recently there have been a number of studies demonstrating that the δ-subunit of the receptor may affect subunit assembly (Korpi et al., 2002) and may also confer differential sensitivity to neurosteroids and to ethanol (Wallner et al., 2003; Wohlfarth et al., 2002).
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