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Key Documents

565785

Sigma-Aldrich

β-Secretase Activity Assay Kit, Fluorogenic

Synonyme(s) :

BACE Activity Assay Kit, Fluorogenic

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About This Item

Code UNSPSC :
41116133

Utilisation

sufficient for 100 tests

Niveau de qualité

Fabricant/nom de marque

Calbiochem®

Conditions de stockage

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

Entrée

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

Méthode de détection

fluorometric

Température de stockage

−20°C

Description générale

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.

Composants

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

Avertissement

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

Principe

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.

Notes préparatoires

• 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.

Stockage et stabilité

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.

Autres remarques

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.

Informations légales

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

Pictogrammes

Health hazardCorrosion

Mention d'avertissement

Danger

Mentions de danger

Classification des risques

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

Code de la classe de stockage

10 - Combustible liquids


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Consulter la Bibliothèque de documents

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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