PC730
Anti-IDE, N-Terminal (97-273) Rabbit pAb
liquid, Calbiochem®
Synonym(s):
Anti-Insulin Degrading Enzyme, Anti-BC2
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100 μL
HUF 189,000.00
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100 μL
HUF 189,000.00
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)
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 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
Markus P Kummer et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 32(49), 17824-17829 (2012-12-12)
Neuroinflammation plays a fundamental role in the pathogenesis of Alzheimer's disease (AD), resulting in the extensive activation of microglial and astroglial cells. Here we describe the role of myeloid-related protein Mrp14, a recently described amplifier of inflammation, in Alzheimer's disease
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