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MAB5206

Sigma-Aldrich

Anti-Beta (β)-Amyloid antibody

CHEMICON®, mouse monoclonal, DE2

别名:

Anti-AAA, Anti-ABETA, Anti-ABPP, Anti-AD1, Anti-APPI, Anti-CTFgamma, Anti-CVAP, Anti-PN-II, Anti-PN2, Anti-alpha-sAPP, Anti-preA4

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About This Item

分類程式碼代碼:
12352203
eCl@ss:
32160702
NACRES:
NA.41

产品名称

抗-淀粉样蛋白抗体，β 1-16，克隆DE2, culture supernatant, clone DE2, Chemicon®

生物源

mouse

品質等級

300

抗體表格

culture supernatant

抗體產品種類

primary antibodies

無性繁殖

DE2, monoclonal

物種活性

monkey, bovine, human

製造商／商標名

Chemicon®

技術

ELISA: suitable
immunohistochemistry: suitable (paraffin)
western blot: suitable

同型

IgG

NCBI登錄號

NM_000484.2
NM_201413.1
NM_201414.1

UniProt登錄號

P05067

運輸包裝

dry ice

目標翻譯後修改

unmodified

基因資訊

human ... APP(351)

應用

抗淀粉样蛋白抗体，β1-16，克隆DE2是一种针对淀粉样蛋白的抗体，用于ELISA、WB、IH(P)。
蛋白质印迹：1:10-1:300免疫组织化学：1:10-1:200在甲醛固定、石蜡包埋的组织上，需要甲酸或微波预处理来染色阿尔兹′海默病大脑老年斑。ELISA免疫沉淀

最佳工作稀释度必须由最终用户确定。

外觀

培养上清液。 含有0.02%叠氮化钠的液体。

法律資訊

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

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儲存類別代碼

10 - Combustible liquids

水污染物質分類（WGK）

WGK 1

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Alexander J Ehrenberg et al.
Acta neuropathologica, 141(5), 651-666 (2021-03-08)
The farnesyltransferase inhibitor, Lonafarnib, reduces tau inclusions and associated atrophy in familial tauopathy models through activation of autophagy, mediated by the inhibition of farnesylation of the Ras GTPase, Rhes. While hinting at a role of Rhes in tau aggregation, it
S100A9 knockout decreases the memory impairment and neuropathology in crossbreed mice of Tg2576 and S100A9 knockout mice model.
Kim, HJ; Chang, KA; Ha, TY; Kim, J; Ha, S; Shin, KY; Moon, C; Nacken, W; Kim, HS; Suh, YH
Testing null
Sandra Grau et al.
Proceedings of the National Academy of Sciences of the United States of America, 102(17), 6021-6026 (2005-04-28)
The defining features of the widely conserved HtrA (high temperature requirement) family of serine proteases are the combination of a catalytic protease domain with one or more C-terminal PDZ domains and reversible zymogen activation. Even though HtrAs have previously been
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Brain communications, 3(2), fcab079-fcab079 (2021-05-21)
Synaptic degeneration has been reported as one of the best pathological correlates of cognitive deficits in Alzheimer's disease. However, the location of these synaptic alterations within hippocampal sub-regions, the vulnerability of the presynaptic versus postsynaptic compartments, and the biological mechanisms

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