Anti-APP monoclonal antibody, clone CBN12

Name: Anti-APP monoclonal antibody, clone CBN12
SKU: DCABH-9603
Rating: 5 (1 reviews)

Mouse Anti-Human APP monoclonal antibody for IHC-P

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COA

SDS

Datasheet

Summary

Specifications

Antibody Isotype

IgG1

Clone

CBN12

Species Reactivity

Human

Immunogen

Synthetic peptide: SGYEVHHQKL, corresponding to amino acids 660-669 of human Amyloid Precursor Protein (which is the same as amino acids 8-17 of the mature Amyloid Protein).

Conjugate

Unconjugated

Target

Alternative Names

APP; amyloid beta (A4) precursor protein; AD1, Alzheimer disease; amyloid beta A4 protein; peptidase nexin II; preA4; protease nexin-II; peptidase nexin-II; beta-amyloid peptide; alzheimer disease amyloid protein; cerebral vascular amyloid peptide; AAA;

Entrez Gene ID

351

UniProt ID

P05067

Product Background

Antigen Description

Functions as a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. Involved in cell mobility and transcription regulation through protein-protein interactions. Can promote transcription activation through binding to APBB1-KAT5 and inhibits Notch signaling through interaction with Numb. Couples to apoptosis-inducing pathways such as those mediated by G(O) and JIP. Inhibits G(o) alpha ATPase activity (By similarity). Acts as a kinesin I membrane receptor, mediating the axonal transport of beta-secretase and presenilin 1. Involved in copper homeostasis/oxidative stress through copper ion reduction. In vitro, copper-metallated APP induces neuronal death directly or is potentiated through Cu(2+)-mediated low-density lipoprotein oxidation. Can regulate neurite outgrowth through binding to components of the extracellular matrix such as heparin and collagen I and IV. The splice isoforms that contain the BPTI domain possess protease inhibitor activity. Induces a AGER-dependent pathway that involves activation of p38 MAPK, resulting in internalization of amyloid-beta peptide and leading to mitochondrial dysfunction in cultured cortical neurons. Provides Cu(2+) ions for GPC1 which are required for release of nitric oxide (NO) and subsequent degradation of the heparan sulfate chains on GPC1.Beta-amyloid peptides are lipophilic metal chelators with metal-reducing activity. Bind transient metals such as copper, zinc and iron. In vitro, can reduce Cu(2+) and Fe(3+) to Cu(+) and Fe(2+), respectively. Beta-amyloid 42 is a more effective reductant than beta-amyloid 40. Beta-amyloid peptides bind to lipoproteins and apolipoproteins E and J in the CSF and to HDL particles in plasma, inhibiting metal-catalyzed oxidation of lipoproteins. Beta-APP42 may activate mononuclear phagocytes in the brain and elicit inflammatory responses. Promotes both tau aggregation and TPK II-mediated phosphorylation. Interaction with Also bind GPC1 in lipid rafts.Appicans elicit adhesion of neural cells to the extracellular matrix and may regulate neurite outgrowth in the brain.The gamma-CTF peptides as well as the caspase-cleaved peptides, including C31, are potent enhancers of neuronal apoptosis.N-APP binds TNFRSF21 triggering caspase activation and degeneration of both neuronal cell bodies (via caspase-3) and axons (via caspase-6).

Pathway

Activated TLR4 signalling, organism-specific biosystem; Advanced glycosylation endproduct receptor signaling, organism-specific biosystem; Alzheimers disease, organism-specific biosystem; Alzheimers disease, conserved biosystem; Amyloids, organism-specific biosystem; Caspase cascade in apoptosis, organism-specific biosystem; Class A/1 (Rhodopsin-like receptors), organism-specific biosystem;

Citations

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Documents

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Q & A

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Q: How do I properly store the Anti-APP monoclonal antibody, clone CBN12 antibody?

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References

New and evolving concepts in the neurotoxicology of lead

TOXICOLOGY AND APPLIED PHARMACOLOGY

Authors: White, L. D.; Cory-Slechta, D. A.; Gilbert, M. E.; Tiffany-Castiglioni, E.; Zawia, N. H.; Virgolini, M.; Rossi-George, A.; Lasley, S. M.; Qian, Y. C.; Basha, Md. Riyaz

Abstract

Lead (Pb) is a xenobiotic metal with no known essential function in cellular growth, proliferation, or signaling. Decades of research characterizing the toxicology of Pb have shown it to be a potent neurotoxicant, especially during nervous system development. New concepts in the neurotoxicology of Pb include advances in understanding the mechanisms and cellular specificity of Pb. Experimental studies have shown that stress can significantly alter the effects of Pb, effects that could potentially be mediated through alterations in the interactions of glucocorticoids with the mesocorticolimbic dopamine system of the brain. Elevated stress, with corresponding elevated glucocorticoid levels, has been postulated to contribute to the increased levels of many diseases and dysfunctions in low socioeconomic status populations. Cellular models of learning and memory have been utilized to investigate the potential mechanisms of Pb-induced cognitive deficits. Examination of long-term potentiation in the rodent hippocampus has revealed Pb-induced increases in threshold, decreases in magnitude, and shorter retention times of synaptic plasticity. Structural plasticity in the form of adult neurogenesis in the hippocampus is also impacted by Pb exposure. The action of Pb on glutamate release, NMDA receptor function, or structural plasticity may underlie perturbations in synaptic plasticity and contribute to learning impairments. In addition to providing insight into potential mechanisms of Pb-induced cognitive deficits, cellular models offer an opportunity to investigate direct effects of Pb on isolated biological substrates. A target of interest is the 78-kDa molecular chaperone glucose-regulated protein (GRP78). GRP78 chaperones the secretion of the cytokine interleukin-6 (IL-6) by astrocytes. In vitro evidence shows that Pb strongly binds to GRP78, induces GRP78 aggregation, and blocks IL-6 secretion in astroglial cells. These findings provide evidence for a significant chaperone deficiency in Pb-exposed astrocytes in culture. In the long term, chaperone deficiency could underlie protein conformational diseases such as Alzheimer's Disease (AD). Lead exposure in early life has been implicated in subsequent progression of amyloidogenesis in rodents during old age. This exposure resulted in an increase in proteins associated with AD pathology viz., beta-amyloid precursor protein (beta-APP), and beta-amyloid (A). These four new lines of research comprise compelling evidence that exposures to Pb have adverse effects on the nervous system, that environmental factors increase nervous system Susceptibility to Pb, and that exposures in early life may cause neurodegeneration in later life. (c) 2007 Elsevier Inc. All rights reserved.

Neuroprotective effects of alpha-lipoic acid on long-term experimental autoimmune encephalomyelitis

EUROPEAN REVIEW FOR MEDICAL AND PHARMACOLOGICAL SCIENCES

Authors: Li, B.; Tan, G. -J.; Lin, H. -Q.; Zhang, J. -N.; Guo, L.; Chen, L. -P.

Abstract

OBJECTIVE: Experimental autoimmune encephalomyelitis (EAE) is an animal model commonly used in research on the acute phase of multiple sclerosis (MS), but studies on the pathology and pathogenesis of EAE with a long disease course are seldom conducted. Besides its antioxidant properties, the comprehensive mechanisms through which alpha-lipoic acid (LA) affects EAE remain obscure. We here conducted the study to explore the possible mechanisms. MATERIALS AND METHODS: In this study. the following methods were used for investigating the effects of LA on long-term EAE: hematoxylin-eosin staining (HE) and electron microscopic examinations of pathological changes: Western blotting of beta-amyloid precursor protein (beta-APP) and myelin basic protein (MBP); Enzyme-linked immunosorbent assay (ELISA) of tumor necrosis factor-alpha (TNF-alpha), transforming growth factor-beta (TGF-beta), superoxide dismutase (SOD), malondialdehyde (MDA) as well as flow cytometry of CD4+CD25+FoxP3+ regulatory T cells (Tregs). RESULTS: The results showed: (1) diverse pathological features of long-term relapsing-remitting EAE; (2) relatively increased MBP and reduced beta-APP expression In LA recipients 180 days after onset; (3) down-regulated TNF-alpha and up-regulated TGF-beta levels in LA recipients 7 days after onset; (4) lower MDA and higher SOD levels in LA recipients 180 days after onset; (5) increased Treg levels in LA recipients 7 days after onset. CONCLUSIONS: Aside from oxidative stress, LA possessed anti-inflammatory and immunomodulatory effects on EAE. LA might be a promising candidate for MS treatment.