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Merck
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MAB5556

Sigma-Aldrich

Anti-Nicastrin Antibody

ascites fluid, clone 9C3, Chemicon®

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About This Item

Código UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41

fonte biológica

mouse

Nível de qualidade

forma do anticorpo

ascites fluid

tipo de produto de anticorpo

primary antibodies

clone

9C3, monoclonal

reatividade de espécies

rat, human, mouse

fabricante/nome comercial

Chemicon®

técnica(s)

immunocytochemistry: suitable
immunoprecipitation (IP): suitable
western blot: suitable

Isotipo

IgG2b

nº de adesão NCBI

nº de adesão UniProt

Condições de expedição

dry ice

modificação pós-traducional do alvo

unmodified

Informações sobre genes

human ... NCSTN(23385)

Especificidade

Nicastrin.

Imunogênio

Synthetic peptide corresponding to the C terminal 18 a.a. of mouse Nicastrin. Due to sequence similarity, it is expected that the antibody will react with most mammals.

Aplicação

Anti-Nicastrin Antibody is an antibody against Nicastrin for use in IP, WB & IC.
Western blot. The antibody recognizes a doublet of ~100-110 kDa. Suggested antibody dilution buffer is TBS with 0.1% Tween-20 and 5% non-fat milk powder. Suggested incubation time is overnight at 2-8°C or 1-2 hours at room temperature.

Immunocytochemistry

Immunoprecipitation. Suggested tissue/cell lysis buffer is 1% Triton X100 or 2% CHAPS. Suggested final reaction volume is 1000 μL with a final protein concentration in the reaction mix of 1 mg/mL. Suggested incubation time is overnight at 2-8°C with rotating. The antibody is known to co-precipitate in CHAPS: presenilin, Aph-1 and Pen-2. Optimal working dilutions must be determined by end user.

Informações legais

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

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Código de classe de armazenamento

10 - Combustible liquids

Classe de risco de água (WGK)

WGK 1

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable


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Jolanta L Lundgren et al.
Journal of neurochemistry, 135(3), 606-615 (2015-08-25)
Synaptic degeneration and accumulation of the neurotoxic amyloid β-peptide (Aβ) in the brain are hallmarks of Alzheimer disease. Aβ is produced by sequential cleavage of the amyloid precursor protein (APP), by the β-secretase β-site APP cleaving enzyme 1 (BACE1) and
Mitsuhiro Inoue et al.
The FEBS journal, 282(14), 2587-2599 (2015-04-22)
The transmembrane protease complex γ-secretase is a key enzyme in Alzheimer disease pathogenesis as it liberates the neurotoxic amyloid β-peptide (Aβ); however, the mechanism of regulation of its activity in various cell types and subcellular compartments is largely unknown. Several
Yasuhiro Teranishi et al.
The FEBS journal, 282(17), 3438-3451 (2015-06-23)
γ-Secretase is a transmembrane protease complex that is responsible for the processing of a multitude of type 1 transmembrane proteins, including the amyloid precursor protein and Notch. γ-Secretase processing of amyloid precursor protein results in the release of the amyloid
gamma-Secretase dependent production of intracellular domains is reduced in adult compared to embryonic rat brain membranes.
Fr?nberg, J; Karlstrom, H; Winblad, B; Tjernberg, LO; Frykman, S
Testing null
Rocío Pérez-González et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 34(9), 12922-12931 (2020-08-11)
Pleiotropic roles are proposed for brain extracellular vesicles (EVs) in the development of Alzheimer's disease (AD). Our previous studies have suggested a beneficial role for EVs in AD, where the endosomal system in vulnerable neurons is compromised, contributing to the

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