癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
Anti-GABAA Receptor α6 Antibody
Our Anti-GABAA Receptor α6 primary antibody from PhosphoSolutions is rabbit polyclonal. It detects m
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Application 
| WB |
|---|---|
| Primary Accession | P30191 |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | IgG |
| Calculated MW | 51184 Da |
| Gene ID | 29708 |
|---|---|
| Other Names | GABA A antibody, GABA A Receptor alphα6 polypeptide antibody, GABA A receptor alphα6 antibody, GABA A receptor subunit alphα6 antibody, GABA subunit A receptor alphα6 antibody, GABA(A) receptor subunit alpha-6 antibody, GABRα6 antibody, GABRA6 antibody, Gamma aminobutyric acid A receptor alphα6 antibody, Gamma aminobutyric acid GABA A receptor alphα6 antibody, Gamma aminobutyric acid receptor subunit alphα6 antibody, Gamma-aminobutyric acid receptor subunit alpha-6 antibody, GBRA6_HUMAN antibody, MGC116903 antibody, MGC116904 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, coexpression 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). Lastly, phosphorylation of β-subunits of the receptor has been shown to modulate GABAA-R function (Brandon et al., 2003). |
| Dilution | WB~~1:1000 |
| Format | Neat 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 α6 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Shipping | Blue Ice |
For Research Use Only. Not For Use In Diagnostic Procedures.
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, coexpression 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). Lastly, phosphorylation of β-subunits of the receptor has been shown to modulate GABAA-R function (Brandon et al., 2003).
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