資料簡介
產(chǎn)品名稱:Rabbit Anti-Utrophin antibody
反應(yīng):Human (predicted: Mouse,Rat,Pig,Sheep,Cow,Chicken,Dog)
免疫原:KLH conjugated synthetic peptide derived from Human Utrophin
單克隆抗體
產(chǎn)品名稱:Anti-Utrophin antibody
Mouse Anti-Utrophin
別名:DMDL; DRP 1; DRP; DRP-1; DRP1; Dystrophin like protein; Dystrophin related protein 1; Dystrophin related protein; Dystrophin-related protein 1; FLJ23678; UTRN; UTRO_HUMAN; Utrophin (homologous to dystrophin); Utrophin
來源:Mouse
克隆類型:Monoclonal
濃度:1mg/ml
亞型:IgG
應(yīng)用: WB=1:1000-1:2000,Elisa=1:1000-1:2000,IHC-P=1:100-500,IHC-F=1:100-500,ICC/IF=1:100-500,IF=1:100-500
反應(yīng): Human
理論分子量:394kDa
免疫原:KLH conjugated synthetic peptide derived from Human Utrophin
保存:-20℃
保質(zhì)期:1年
Dystrophin and utrophin are related structural, Actin-binding proteins that are involved in anchoring the cytoskeleton to the plasma membrane. Dystrophin is the protein product of the Duchenne/Becker muscular dystrophy gene. Dystrophin expression is found in muscle and brain tissues, where it is localized to the inner surface of the plasma membrane. It has been speculated that alternative splicing of the carboxy terminus allows dystrophin to interact with a variety of proteins. Research has shown that the loss of dystrophin-associated proteins in Duchenne afflicted muscle is due to the absence of dystrophin rather than to muscle degradation and that the lack of dystrophin results in the loss of linkage between the cytoskeleton and the extracellular matrix. Evidence suggests that the upregulation of utrophin can reduce the dystrophic pathology.
應(yīng)用:SDS-PAGE,Western blot,ELISA
Biological activity,immunology research
Dystrophin and utrophin are related structural, Actin-binding proteins that are involved in anchoring the cytoskeleton to the plasma membrane. Dystrophin is the protein product of the Duchenne/Becker muscular dystrophy gene. Dystrophin expression is found in muscle and brain tissues, where it is localized to the inner surface of the plasma membrane. It has been speculated that alternative splicing of the carboxy terminus allows dystrophin to interact with a variety of proteins. Research has shown that the loss of dystrophin-associated proteins in Duchenne afflicted muscle is due to the absence of dystrophin rather than to muscle degradation and that the lack of dystrophin results in the loss of linkage between the cytoskeleton and the extracellular matrix. Evidence suggests that the upregulation of utrophin can reduce the dystrophic pathology.
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