Anti-APP (aa 1-16) polyclonal antibody

Name: Anti-APP (aa 1-16) polyclonal antibody
SKU: DPABH-25223
Rating: 5 (1 reviews)

Goat Anti-Human APP (aa 1-16) polyclonal antibody for WB

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COA

SDS

Datasheet

Summary

Specifications

Antibody Isotype

IgG

Species Reactivity

Mouse; Human

Immunogen

Synthetic peptide: DAEFRHDSGYEVHHQK-C with a Cysteine residue linker, corresponding to N terminal amino acids 1-16 of Human beta Amyloid (NP_000475.1; NP_958816.1; NP_958817.1; NP_001129601.1; NP_001129602.1).

Conjugate

Unconjugated

Applications

Application Notes

WB: 1 - 3μg/ml

Target

Alternative Names

APP; amyloid beta (A4) precursor protein; AAA; AD1; PN2; ABPP; APPI; CVAP; ABETA; PN-II; CTFgamma; amyloid beta A4 protein; preA4; protease nexin-II; peptidase nexin-II; beta-amyloid peptide; alzheimer disease amyloid protein; cerebral vascular amyloid pe

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.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 overexpressed HADH2 leads to oxidative stress and neurotoxicity.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; Alzheimers disease; Alzheimers Disease; Caspase cascade in apoptosis

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Lithium Reduces BACE1 Overexpression, Beta Amyloid Accumulation, and Spatial Learning Deficits in Mice with Traumatic Brain Injury

JOURNAL OF NEUROTRAUMA

Authors: Yu, Fengshan; Zhang, Yumin; Chuang, De-Maw

Abstract

Traumatic brain injury (TBI) leads to both acute injury and long-term neurodegeneration, and is a major risk factor for developing Alzheimer's disease (AD). Beta amyloid (A beta) peptide deposits in the brain are one of the pathological hallmarks of AD. A beta levels increase after TBI in animal models and in patients with head trauma, and reducing A beta levels after TBI has beneficial effects. Lithium is known to be neuroprotective in various models of neurodegenerative disease, and can reduce A beta generation by modulating glycogen synthase kinase-3 (GSK-3) activity. In this study we explored whether lithium would reduce A beta load after TBI, and improve learning and memory in a mouse TBI model. Lithium chloride (1.5 mEq/kg, IP) was administered 15 min after TBI, and once daily thereafter for up to 3 weeks. At 3 days after injury, lithium attenuated TBI-induced A beta load increases, amyloid precursor protein (APP) accumulation, and beta-APP-cleaving enzyme-1 (BACE1) overexpression in the corpus callosum and hippocampus. Increased Tau protein phosphorylation in the thalamus was also attenuated after lithium treatment following TBI at the same time point. Notably, lithium treatment significantly improved spatial learning and memory in the Y-maze test conducted 10 days after TBI, and in the Morris water maze test performed 17-20 days post-TBI, in association with increased hippocampal preservation. Thus post-insult treatment with lithium appears to alleviate the TBI-induced A beta load and consequently improves spatial memory. Our findings suggest that lithium is a potentially useful agent for managing memory impairments after TBI or other head trauma.

Andrographolide - A promising therapeutic agent, negatively regulates glial cell derived neurodegeneration of prefrontal cortex, hippocampus and working memory impairment

JOURNAL OF NEUROIMMUNOLOGY

Authors: Das, Sudeshna; Mishra, K. P.; Ganju, Lilly; Singh, S. B.

Abstract

Over activation of glial cell derived innate immune factors induces neuro-inflammation that results in neurodegenerative disease, like working memory impairment. In this study, we have investigated the role of andrographolide, a major constituent of Andrographis paniculata plant, in reduction of reactive glial cell derived working memory impairment. Real time PCR, Western bloting, flow cytometric and immunofluorescence studies demonstrated that andrographolide inhibited lipopolysaccharide (LPS)-induced overexpression of HMGB1, TLR4, NF kappa B, COX-2, iNOS, and release of inflammatory mediators in primary mix glial culture, adult mice prefrontal cortex and hippocampus region. Active microglial and reactive astrocytic makers were also down regulated after andrographolide treatment. Andrographolide suppressed overexpression of microglial MIP-1 alpha, P2X7 receptor and its downstream signaling mediators including-inflammasome NLRP3, caspasel and mature IL-1 beta. Furthermore, in vivo maze studies suggested that andrographolide treatment reversed LPS-induced behavioural and working memory disturbances including regulation of expression of protein markers like PKC, p-CREB, amyloid beta, APP, p-tau, synapsin and PSD-95. Andrographolide, by lowering expression of pro apoptotic genes and enhancing the expression of anti-apoptotic gene showed its anti-apoptotic nature that in turn reduces neurodegeneration. Morphology studies using Nissl and FJB staining also showed the neuroprotective effect of andrographolide in the prefrontal cortex region. The above studies indicated that andrographolide prevented neuroinflammation-associated neurodegeneration and improved synaptic plasticity markers in cortical as well as hippocampal region which suggests that andrographolide could be a novel pharmacological countermeasure for the treatment of neuroinflammation and neurological disorders related to memory impairment.