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Anti-Human BCR/ABL Polyclonal Antibody (HP839014)

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概要
カタログ番号HP839014
種反応性Human, Mouse
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 BCR/ABL (Gln1-Cys97).
ターゲット BCR/ABL p210 fusion protein, BCR/ABL fusion
精製 Purified by antigen affinity column.
アクセッション番号 P00520, P00519
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

Tyrosine-protein kinase ABL1 (BCR) is a ~122 kDa protein. Non-receptor tyrosine-protein kinase that plays a role in many key processes linked to cell growth and survival such as cytoskeleton remodeling in response to extracellular stimuli, cell motility and adhesion, receptor endocytosis, autophagy, DNA damage response and apoptosis. Coordinates actin remodeling through tyrosine phosphorylation of proteins controlling cytoskeleton dynamics like WASF3 (involved in branch formation); ANXA1 (involved in membrane anchoring); DBN1, DBNL, CTTN, RAPH1 and ENAH (involved in signaling); or MAPT and PXN (microtubule-binding proteins). Phosphorylation of WASF3 is critical for the stimulation of lamellipodia formation and cell migration. Involved in the regulation of cell adhesion and motility through phosphorylation of key regulators of these processes such as BCAR1, CRK, CRKL, DOK1, EFS or NEDD9. Phosphorylates multiple receptor tyrosine kinases and more particularly promotes endocytosis of EGFR, facilitates the formation of neuromuscular synapses through MUSK, inhibits PDGFRB-mediated chemotaxis and modulates the endocytosis of activated B-cell receptor complexes.

1. Chen, A. et al. (2011) Molecular and cellular biology 31, 3445-56. PMID: 21690296
2. Gu, JJ. et al. (2012) Science signaling 5, ra51. PMID: 22810897
注意事項 For research use only.
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参考文献
Formula
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