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Merck

565785

Sigma-Aldrich

β-Secretase Activity Assay Kit, Fluorogenic

別名:

BACE Activity Assay Kit, Fluorogenic

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About This Item

UNSPSCコード:
41116133

使用法

sufficient for 100 tests

品質水準

メーカー/製品名

Calbiochem®

保管条件

OK to freeze
avoid repeated freeze/thaw cycles
protect from light

入力

sample type tissue extract(s)
sample type purified enzyme(s) (BACE)
sample type cell lysate

検出方法

fluorometric

保管温度

−20°C

詳細

A sensitive fluorogenic assay kit for the determination of β-secretase (BACE) activity (Excitation max: 335-355 nm; Emission max: 495-501 nm). β-Secretase is a transmembrane aspartyl protease that cleaves membrane-bound amyloid precursor protein.

構成

Extraction Buffer, Reaction Buffer, β-Secretase Substrate, β-Secretase Protein (Positive Control), β-Secretase Inhibitor, and a user protocol.

警告

Toxicity: Multiple Toxicity Values, refer to MSDS (O)

原理

The Calbiochem β-Secretase Activity Assay Kit, Fluorogenic, is intended for measuring the β-secretase (BACE) activity in cell lysates, tissue extracts, or purified enzyme preparations.

調製ノート

• Active β-Secretase: Reconstitute the lyophilized Active β-Secretase with 10 µl ddH2O. Following reconstitution, aliquot and freeze (-70°C) to avoid loss of activity.

保管および安定性

Upon arrival store the entire contents of the kit at -20°C. Following reconstitution of the Active β-Secretase, aliquot and freeze (-70°C) to avoid loss of activity. Following initial thaw of the kit contents, store the Extraction Buffer and 2X Reaction Buffer at 4°C.

その他情報

Due to the nature of the Hazardous Materials in this shipment, additional shipping charges may be applied to your order. Certain sizes may be exempt from the additional hazardous materials shipping charges. Please contact your local sales office for more information regarding these charges.

法的情報

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

ピクトグラム

Health hazardCorrosion

シグナルワード

Danger

危険有害性情報

危険有害性の分類

Eye Dam. 1 - Muta. 2 - Skin Irrit. 2

保管分類コード

10 - Combustible liquids


適用法令

試験研究用途を考慮した関連法令を主に挙げております。化学物質以外については、一部の情報のみ提供しています。 製品を安全かつ合法的に使用することは、使用者の義務です。最新情報により修正される場合があります。WEBの反映には時間を要することがあるため、適宜SDSをご参照ください。

Jan Code

565785-1KIT:
565785-PKIT:


試験成績書(COA)

製品のロット番号・バッチ番号を入力して、試験成績書(COA) を検索できます。ロット番号・バッチ番号は、製品ラベルに「Lot」または「Batch」に続いて記載されています。

以前この製品を購入いただいたことがある場合

文書ライブラリで、最近購入した製品の文書を検索できます。

文書ライブラリにアクセスする

Divna Lazic et al.
The Journal of experimental medicine, 216(2), 279-293 (2019-01-17)
3K3A-activated protein C (APC), a cell-signaling analogue of endogenous blood serine protease APC, exerts vasculoprotective, neuroprotective, and anti-inflammatory activities in rodent models of stroke, brain injury, and neurodegenerative disorders. 3K3A-APC is currently in development as a neuroprotectant in patients with
Lei Liu et al.
The Journal of cell biology, 218(2), 644-663 (2019-01-11)
Intramembrane proteolysis of transmembrane substrates by the presenilin-γ-secretase complex is preceded and regulated by shedding of the substrate's ectodomain by α- or β-secretase. We asked whether β- and γ-secretases interact to mediate efficient sequential processing of APP, generating the amyloid
Crystal D Hayes et al.
BMC medicine, 11, 81-81 (2013-03-28)
Currently available therapies for Alzheimer's disease (AD) do not treat the underlying cause of AD. Anecdotal observations in nursing homes from multiple studies strongly suggest an inverse relationship between cancer and AD. Therefore, we reasoned that oncology drugs may be
Yan Cai et al.
Neurotoxicity research, 21(2), 160-174 (2011-07-05)
β-amyloid precursor protein (APP) and presenilins mutations cause early-onset familial Alzheimer's disease (FAD). Some FAD-based mouse models produce amyloid plaques, others do not. β-Amyloid (Aβ) deposition can manifest as compact and diffuse plaques; it is unclear why the same Aβ
Xue-Mei Zhang et al.
The European journal of neuroscience, 31(4), 710-721 (2010-04-14)
Cerebral hypometabolism and amyloid accumulation are principal neuropathological manifestations of Alzheimer's disease (AD). Whether and how brain/neuronal activity might modulate certain pathological processes of AD are interesting topics of recent clinical and basic research in the field, and may be

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