Human APP blocking peptide (CDBP0394)

Synthetic Human APP blocking peptide for BL, IHC

Product Overview
APP ( N - term ) peptide ( human )
Target
Amyloid Precursor Protein
Nature
Synthetic
Species Reactivity
Human
Tag/Conjugate
Unconjugated
Procedure
None
Concentration
0.2 mg/ml
Size
50 μg
Buffer
PBS with 0.1% BSA 0.02% sodium azide pH7.2
Preservative
0.02% Sodium Azide
Storage
Upon receipt - Keep as concentrated solution. Aliquot and store at -20℃ or below. Avoid freeze-thaw cycles.
UniProt ID
Antigen Description
This gene encodes a cell surface receptor and transmembrane precursor protein that is cleaved by secretases to form a number of peptides. Some of these peptides are secreted and can bind to the acetyltransferase complex APBB1/TIP60 to promote transcriptional activation, while others form the protein basis of the amyloid plaques found in the brains of patients with Alzheimer disease. Mutations in this gene have been implicated in autosomal dominant Alzheimer disease and cerebroarterial amyloidosis (cerebral amyloid angiopathy). Multiple transcript variants encoding several different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]
Function
DNA binding; PTB domain binding; acetylcholine receptor binding; growth factor receptor binding; heparin binding; identical protein binding; peptidase activator activity; protein binding; receptor binding; serine-type endopeptidase inhibitor activity; tra
Synonyms
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 peptide;

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References


Osmotin attenuates LPS-induced neuroinflammation and memory impairments via the TLR4/NF kappa B signaling pathway

SCIENTIFIC REPORTS

Authors: Badshah, Haroon; Ali, Tahir; Kim, Myeong Ok

Toll-like receptor 4 (TLR4) signaling in the brain mediates autoimmune responses and induces neuroinflammation that results in neurodegenerative diseases, such as Alzheimer's disease (AD). The plant hormone osmotin inhibited lipopolysaccharide (LPS)-induced TLR4 downstream signaling, including activation of TLR4, CD14, IKK alpha/beta, and NF kappa B, and the release of inflammatory mediators, such as COX-2, TNF-alpha, iNOS, and IL-1 beta. Immunoprecipitation demonstrated colocalization of TLR4 and AdipoR1 receptors in BV2 microglial cells, which suggests that osmotin binds to AdipoR1 and inhibits downstream TLR4 signaling. Furthermore, osmotin treatment reversed LPS-induced behavioral and memory disturbances and attenuated LPS-induced increases in the expression of AD markers, such as A beta, APP, BACE-1, and p-Tau. Osmotin improved synaptic functionality via enhancing the activity of pre-and post-synaptic markers, like PSD-95, SNAP-25, and syntaxin-1. Osmotin also prevented LPS-induced apoptotic neurodegeneration via inhibition of PARP-1 and caspase-3. Overall, our studies demonstrated that osmotin prevented neuroinflammation-associated memory impairment and neurodegeneration and suggest AdipoR1 as a therapeutic target for the treatment of neuroinflammation and neurological disorders, such as AD.

Kinematics of the parsec-scale radio jet in 3C 48

MONTHLY NOTICES OF THE ROYAL ASTRONOMICAL SOCIETY

Authors: An, T.; Hong, X. Y.; Hardcastle, M. J.; Worrall, D. M.; Venturi, T.; Pearson, T. J.; Shen, Z. -Q.; Zhao, W.; Feng, W. X.

We present results on the compact steep-spectrum quasar 3C 48 from observations with the Very Long Baseline Array (VLBA), the Multi-Element Radio Linked Interferometer Network (MERLIN) and the European Very long baseline interferometry (VLBI) Network (EVN) at multiple radio frequencies. In the 1.5-GHz VLBI images, the radio jet is characterized by a series of bright knots. The active nucleus is embedded in the southernmost VLBI component A, which is further resolved into two sub-components A1 and A2 at 4.8 and 8.3 GHz, respectively. A1 shows a flat spectrum and A2 shows a steep spectrum. The most strongly polarized VLBI components are located at component C similar to 0.25 arcsec north of the core, where the jet starts to bend to the north-east. The polarization angles at C show gradual changes across the jet width at all observed frequencies, indicative of a gradient in the emission-weighted intrinsic polarization angle across the jet and possibly a systematic gradient in the rotation measure; moreover, the percentage of polarization increases near the curvature at C, likely consistent with the presence of a local jet-interstellar-medium interaction and/or changing magnetic-field directions. The hot spot B shows a higher rotation measure, and has no detected proper motion. These facts provide some evidence for a stationary shock in the vicinity of B. Comparison of the present VLBI observations with those made 8.43 yr ago suggests a significant northward motion for A2 with an apparent transverse velocity beta(app) = 3.7 +/- 0.4c. The apparent superluminal motion suggests that the relativistic jet plasma moves at a velocity of greater than or similar to 0.96c if the jet is viewed at an inclination angle less than 20 degrees. A simple precessing jet model and a hydrodynamical isothermal jet model with helical-mode Kelvin-Helmholtz instabilities are used to fit the oscillatory jet trajectory of 3C 48 defined by the bright knots.

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