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PC730

Sigma-Aldrich

Anti-IDE, N-Terminal (97-273) Rabbit pAb

liquid, Calbiochem®

Synonym(s):

Anti-Insulin Degrading Enzyme, Anti-BC2

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

antibody form

serum

antibody product type

primary antibodies

clone

polyclonal

form

liquid

contains

≤0.1% sodium azide as preservative

species reactivity

rat, human, hamster, mouse

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
avoid repeated freeze/thaw cycles

isotype

IgG

shipped in

wet ice

storage temp.

−70°C

target post-translational modification

unmodified

Gene Information

human ... IDE(3416)

General description

Rabbit polyclonal antibody supplied as undiluted serum. Recognizes the ~115 kDa endogenous as well as recombinant IDE protein.
Recognizes the ~115 kDa endogenous and recombinant IDE.
This Anti-IDE, N-Terminal (97-273) Rabbit pAb is validated for use in ELISA, Immunoblotting, Immunocytochemistry, Immunoprecipitation for the detection of IDE, N-Terminal (97-273).

Immunogen

Rat
a recombinant protein consisting of amino acids 97-273 of rat IDE fused to GST

Application

ELISA (direct only) (1:2000-1:4000)

Immunoblotting (1:500-1:4000)

Immunocytochemistry (1:200-1:1000)

Immunoprecipitation (not recommended)

Warning

Toxicity: Standard Handling (A)

Physical form

Undiluted serum.

Reconstitution

Following initial thaw, aliquot and freeze (-70°C).

Analysis Note

Positive Control
Rat or mouse liver cytosol

Other Notes

Antibody should be titrated for optimal results in individual systems.
Morelli, L., et al. 2003. J. Biol. Chem.278, 23221.
Kurochkin, I.V. and Goto, S. 1994. FEBS Lett.345, 33.

Legal Information

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

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Storage Class Code

10 - Combustible liquids

WGK

WGK 1


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Markus P Kummer et al.
Neuron, 71(5), 833-844 (2011-09-10)
Part of the inflammatory response in Alzheimer's disease (AD) is the upregulation of the inducible nitric oxide synthase (NOS2) resulting in increased NO production. NO contributes to cell signaling by inducing posttranslational protein modifications. Under pathological conditions there is a
Jeong-Eun Lim et al.
The American journal of pathology, 179(3), 1095-1103 (2011-07-19)
The accumulation of β-amyloid protein (Aβ) in the brain is thought to be a primary etiologic event in Alzheimer's disease (AD). Fibrillar Aβ plaques, a hallmark of AD abnormality, are closely associated with activated microglia. Activated microglia have contradictory roles
Shaowu Cheng et al.
The Journal of biological chemistry, 288(50), 35952-35960 (2013-10-19)
Isoprenoids and prenylated proteins have been implicated in the pathophysiology of Alzheimer disease (AD), including amyloid-β precursor protein metabolism, Tau phosphorylation, synaptic plasticity, and neuroinflammation. However, little is known about the relative importance of the two protein prenyltransferases, farnesyltransferase (FT)
Lixia Zhao et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 24(49), 11120-11126 (2004-12-14)
Insulin-degrading enzyme (IDE) is one of the proteins that has been demonstrated to play a key role in degrading beta-amyloid (Abeta) monomer in vitro and in vivo, raising the possibility of upregulating IDE as an approach to reduce Abeta. Little
Juan José Ramos-Rodriguez et al.
Molecular neurobiology, 53(4), 2685-2697 (2015-07-15)
Alzheimer's disease (AD) and vascular dementia (VaD) are the most common causes of dementia, and borderlines are blurred in many cases. Aging remains the main risk factor to suffer dementia; however, epidemiological studies reveal that diabetes may also predispose to

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