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Anti-GNA11 Polyclonal Antibody (HB814014)

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概要
カタログ番号HB814014
説明
Anti-GNA11 Polyclonal Antibody (HB814014) is a rabbit polyclonal antibody detecting GNA11 in ELISA, IHC, WB. Suitable for Human, Mouse, Dog, Rat, and Bovine.
Highlights
  • ●Affinity Purified — Minimal background and high purity for reliable results.
  • ●Multi-Application — Validated across multiple applications.
  • ●Multi-Species — Cross-reactive for translational research.
種反応性Human, Mouse, Rat
アプリケーションELISA, IHC, WB
宿主種Rabbit
クローン性Polyclonal
アイソタイプIgG
免疫原 E. coli - derived recombinant Human GNA11 (Met1-Val359).
ターゲット G-protein subunit alpha-11, Guanine nucleotide-binding protein G(y) subunit alpha, GNA11, G alpha-11, GA11, Guanine nucleotide-binding protein subunit alpha-11
精製 Purified by antigen affinity column.
アクセッション番号 P29992
形態 Liquid
保存バッファー 0.01M PBS, pH 7.4, 50% Glycerol, 0.05% Proclin 300.

データシートのハードコピーまたはロット固有のCOAに記載された具体的なバッファー情報を参照してください。

製品使用情報
アプリケーション 希釈
ELISA 1:5000-1:20000
IHC 1:50-1:500
WB 1:500-1:2000
安定性と保存 Use a manual defrost freezer and avoid repeated freeze thaw cycles. Store at 2 to 8°C for frequent use. Store at -20 to -80°C for twelve months from the date of receipt.
背景

Guanine nucleotide-binding protein subunit alpha-11 (GNA11) is a ~42 kDa protein. Guanine nucleotide-binding proteins (G proteins) function as transducers downstream of G protein-coupled receptors (GPCRs) in numerous signaling cascades. The alpha chain contains the guanine nucleotide binding site and alternates between an active, GTP-bound state and an inactive, GDP-bound state. Signaling by an activated GPCR promotes GDP release and GTP binding. The alpha subunit has a low GTPase activity that converts bound GTP to GDP, thereby terminating the signal. Both GDP release and GTP hydrolysis are modulated by numerous regulatory proteins.

1. Maeda, S. et al. (2019) Science (New York, N.Y.) 364, 552-557. PMID: 31073061
2. Alvarez-Curto, E. et al. (2016) The Journal of biological chemistry 291, 27147-27159. PMID: 27852822
注意事項 For research use only.
イメージ
参考文献
Formula
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