|Calculated MW||52 KDa|
|Other Names||Gamma-aminobutyric acid receptor subunit delta, GABA(A) receptor subunit delta, Gabrd|
|Target/Specificity||Fusion protein from the N-terminal region of the delta subunit.|
|Format||Prepared from rabbit serum by affinity purification using a column to which the fusion protein immunogen was coupled|
|Antibody Specificity||Specific for the ~52k δ-subunit of the GABAA receptor|
|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||GABAA Receptor, δ-Subunit, N-Terminus Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
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Provided below are standard protocols that you may find useful for product applications.
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 GABAA receptor (GABAA-R) subtype. GABAA-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 GABAA-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 GABAA-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 α-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).
Korpi ER, Mihalek RM, Sinkkonen ST, Hauer B, Hevers W, Homanics GE, Sieghart W, Luddens H (2002) Altered receptor subtypes in the forebrain of GABAA receptor δ-subunit-deficient mice: recruitment of γ2-subunits. Neurosci 109:733-743.
McKernan RM, et al. (2000) Sedative but not anxiolytic properties of benzodiazepines are mediated by the GABAA receptor α1-subtype. Nature Neurosci 3:587-592.
Mehta AK, Ticku MK (1998) Prevalence of the GABAA receptor assemblies containing α1-subunit in the rat cerebellum and cerebral cortex as determined by immunoprecipitation: Lack of modulation by chronic ethanol administration. Mol Brain Res 67:194-199.
Ogris W, Pöltl A, Hauer B, Ernst M, Oberto A, Wulff P, Höger H, Wisden W, Sieghart W (2004) Affinity of various benzodiazepine site ligands in mice with a point mutation in the GABAA receptor γ2-subunit. Biochem Pharmacol 68:1621-1629.
Olsen RW, Tobin AJ (1990) Molecular biology of GABAA receptors. FASEB 4:1469-1480.
Pöltl A, Hauer B, Fuchs K, Tretter V, Sieghart W (2003) Subunit composition and quantitative importance of GABAA receptor subtypes in the cerebellum of mouse and rat. J Neurochem 87:1444-1455.
Wallner M, Hanchar HJ, Olsen RW (2003) From The Cover: Ethanol enhances α4β3δ and α6β3δ γ-aminobutyric acid type A receptors at low concentrations known to affect humans. Proc Natl Acad Sci (USA) 100:15218-15223.
Whiting PJ, Bonnert TP, McKernan RM, Farrar S, Le Bourdellès B, Heavens RP, Smith DW, Hewson L, Rigby MR, Sirinathsinghji DJS, Thompson SA, Wafford KA (1999) Molecular and functional diversity of the expanding GABAA receptor gene family. Ann NY Acad Sci 868:645-653.
Wohlfarth KM, Bianchi MT, Macdonald RL (2002) Enhanced Neurosteroid Potentiation of Ternary GABAA Receptors Containing the δ-Subunit. J Neurosci 22:1541-1549.
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