PC730
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
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)
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
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.
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
10 - Combustible liquids
wgk_germany
WGK 1
Certificates of Analysis (COA)
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I V Kurochkin et al.
FEBS letters, 345(1), 33-37 (1994-05-23)
Cerebral deposition of beta-amyloid peptide (beta A) is a hallmark of Alzheimer's disease. Concentration of beta A could play a critical role in the rate of amyloid deposition. It is therefore of considerable importance to identify proteases involved in processing
Xiqian Lan et al.
Journal of immunology (Baltimore, Md. : 1950), 186(12), 6925-6932 (2011-05-10)
The advent and wide introduction of antiretroviral therapy has greatly improved the survival and longevity of HIV-infected patients. Unfortunately, despite antiretroviral therapy treatment, these patients are still afflicted with many complications including cognitive dysfunction. There is a growing body of
Laura Morelli et al.
The Journal of biological chemistry, 278(26), 23221-23226 (2003-04-16)
Inherited amino acid substitutions at position 21, 22, or 23 of amyloid beta (Abeta) lead to presenile dementia or stroke. Insulin-degrading enzyme (IDE) can hydrolyze Abeta wild type, yet whether IDE is capable of degrading Abeta bearing pathogenic substitutions is
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
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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