Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
Human APP Protein expressed in HEK-293 Cells - ABIN2714676
Planque, Nishiyama, Sonoda, Lin, Taguchi, Hara, Kolodziej, Mitsuda, Gonzalez, Sait, Fukuchi, Massey, Friedland, ONuallain, Sigurdsson, Paul: Specific amyloid β clearance by a catalytic antibody construct. in The Journal of biological chemistry 2015
Results show that Drosophila APPL-RNAi largely mimics transgenic amyloid beta in various phenotypes which include eye degeneration, reduced longevity and motor neuron deficit functions. This is the first report showing comparable phenotypes between APPL and amyloid beta in Alzheimer's disease model of Drosophila.
Appl siRNA inhibition in cortex glia resulted in longer sleep and reduced expression of genes involved in glutamate (show GRIN2A Proteins) recycling.
memory is altered by two connected mechanisms-APPL loss-of-function and amyloid peptide toxicity-revealing in Drosophila a functional interaction between APPL and amyloid peptide.
Our data demonstrate that, in addition to secreted APPL, the noncleaved form is involved in memory, raising the possibility that secreted and full-length APPL act together in memory processes.
findings suggest that a normal function of presenilin (PS)is to repress kinesin-1 and dynein motor activity during axonal transport of amyloid precursor protein (APP) vesicles; perturbations of APP/PS transport could contribute to early neuropathology observed in Alzheimer's Disease
APPL is the first example of a modulator of the Wnt (show WNT4 Proteins)-PCP (show PRCP Proteins) pathway specifically required for axon outgrowth.
Data show that Appl is directly regulated by the Ras/MAPK (show MAPK1 Proteins) pathway through a mechanism mediated by PntP2 (show ETS2 Proteins).
[review] APP-like proteins are involved in neuronal differentiation, neuritic outgrowth, and synapse formation.
Disruption of amyloid protein (show IAPP Proteins) precursor (APP) proteins and specifically their soluble alpha-cleaved ectodomains can protect against progressive neurodegeneration in vivo.
Down-regulation of the ATP-binding cassette transporter 2 (Abca2 (show ABCA2 Proteins)) reduces amyloid-beta production by altering Nicastrin (show NCSTN Proteins) maturation and intracellular localization.
BECN1 (show BECN1 Proteins)-APP association and BECN1 (show BECN1 Proteins)-dependent APP endocytosis and degradative trafficking were negatively regulated by active AKT (show AKT1 Proteins).
The authors demonstrate that pathological PS1 (show PSEN1 Proteins) loss-of-function impinges on neurite formation through a selective APP gain-of-function that could impact on axodendritic connectivity and contribute to aberrant axonal sprouting observed in Alzheimer's disease patients.
These findings thus provide new insights into Abeta-induced mitochondrial defects that may contribute to neuronal dysfunction and Alzheimer's disease pathogenesis.
Results show that Drosophila APPL (show APPL1 Proteins)-RNAi largely mimics transgenic amyloid beta in various phenotypes which include eye degeneration, reduced longevity and motor neuron deficit functions. This is the first report showing comparable phenotypes between APPL (show APPL1 Proteins) and amyloid beta in Alzheimer's disease model of Drosophila.
ABETA oxidation by the Cu-ABETA complex triggers a positive feedback loop that leads to a more deleterious oxidative stress due to both an enhanced reactive oxygen species production rate and a decreased HO scavenging ability.
both apolipoprotein E (show APOE Proteins) and Abeta1-42 abundance can differ depending upon the type of CJD (show PRNP Proteins).
APP substrate occupancy of these three pockets of gamma-secretase occurs after initial substrate binding but precedes catalysis, suggesting a conformational change in substrate may be required for cleavage.
Results show that concerted signaling by both APP and Abeta is necessary for aberrant neuronal cell cycle entry. Thus, APP plays a central role in promotion of neurodegeneration, through activation of Ras-ERK signaling axis as well as GSK-3, and interfering with these signaling events would impede cell cycle reentry and neurodegeneration observed in Alzheimer's disease.
These results provide an unprecedented view of how albumin (show ALB Proteins) interacts with Abeta and illustrate the potential of dark-state exchange saturation transfer NMR in mapping the interactions between amyloid-inhibitory proteins and amyloidogenic peptides.
Study demonstrates the effect of betaAPP/Abeta on the metabolism of arginine, shows for the first time that betaAPP/Abeta simultaneously down-regulated both arginases and increased constitutive NOS (show NOS1 Proteins) isoforms, suggests that the significance of arginases for the promotion of NOS (show NOS1 Proteins)-dependent cellular stress by betaAPP/Abeta in a system where up-regulated, potentially pathogenic miRNAs are involved.
Amyloid-beta inhibits No-cGMP signaling in a CD36 (show CD36 Proteins)- and CD47 (show CD47 Proteins)-dependent manner
These experiments demonstrate the roles of Chol and ApoE (show APOE Proteins) in the modulation of membrane insertion of APP.
Two novel transcript variants of porcine APP have been identified, producing isoforms of 695 and 751 amino acids, respectively.
APP could be acting through a semaphorin receptor as well
This study describes Abeta deposition in 102 clinically characterized cattle brains from animals aged 0 to 20 years, demonstrates certain similarities between Abeta deposition patterns exhibited in cattle brains and those in the human brain in early stages of aging
release and aggregation of amyloid beta-peptide from brain lipid bilayers is regulated by cholesterol and GM1
The authors concluded that the FcgammaRIIb-SHIP2 (show INPPL1 Proteins) axis links Abeta neurotoxicity to tau pathology by dysregulating phosphoinositide metabolism, providing insight into therapeutic potential against Alzheimer's disease.
results suggest that PrP(C (show PRNP Proteins)) recognizes structural features common to both Abeta oligomers and fibril ends and that this interaction could contribute to the neurotoxic effect of Abeta aggregates.
Transmembrane APP expressed by tumor cells binds to endothelial DR6 (show TNFRSF21 Proteins) to trigger necroptosis, and targeting DR6 (show TNFRSF21 Proteins)-mediated endothelial cell necroptosis may be a potential therapeutic strategy
Our study provides the first direct evidence that Abeta, an AD-linked factor, is associated to the pathogenesis of ALS and provides molecular clues to understand common aggregation mechanisms in the pathogenesis of neurodegenerative diseases.
Although hyperactivity and hypersynchronicity were respectively detected in mice expressing the PS2 (show PDCD6 Proteins)-N141I or the APP Swedish mutant alone, the increase in cross-frequency coupling specifically characterized the 6-month-old PS2APP mice, just before the surge of the cognitive decline
these results uncover a novel role for mDia1 in Abeta-mediated synaptotoxicity and demonstrate that inhibition of MT dynamics and accumulation of PTMs are driving factors for the induction of tau-mediated neuronal damage.
APP and its metabolites are capable of influencing the basic physiology of the pancreas.
treatment of APP/E4/Abca1+/- mice with liver X receptor (LXR) agonist T0 ameliorates APOE4-induced Alzheimer's disease (AD)-like pathology and therefore targeting the LXR-ABCA1-APOE regulatory axis could be effective as a potential therapeutic approach in AD patients, carriers of APOEepsilon4
These results provide evidence supporting a key role for the p38 MAPK (show MAPK14 Proteins) signaling pathway which is involved in the regulation of Abeta1-42 internalization in the parietal cortex and hippocampus of mouse through LRP1 (show LRP1 Proteins) in vivo.
increased APP and/or beta-CTF impact the endocytic pathway to disrupt NGF trafficking and signaling, resulting in trophic deficits in basal forebrain cholinergic neurons.
Report of biosynthesis of APP in physiological context and illuminate occurrence of two pools of APP, one of which is linked to neuroendocrine cell activation.
A "CAGA (show S100A8 Proteins)" sequence proximal to the "ATG" start codon & immediately upstream of an interleukin-1-responsive element was found in a location unique to APP genes of amyloid plaque-forming species & absent in all other genes surveyed.
endogenous cleavages at prohormone convertase-like sites in APP
Amyloid beta precursor protein and prion protein (show PRNP Proteins) have a conserved interaction affecting cell adhesion and central nervous system development.
A reduction in app levels causes defective axonal outgrowth of facial branchiomotor and spinal motor neurons, which involves disorganized axonal cytoskeletal elements.
these results indicate the Appa-RFP (show MKRN1 Proteins) and Aplp2 (show APLP2 Proteins) fusion proteins are likely secreted from the central nervous system and accumulate in the embryonic veins independent of blood flow.
Data show that knock down of APP in zebrafish results in fish with reduced body length and a short, curly tail, and that wild-type human APP rescues the morphant phenotype, but the Swedish mutant APP, which causes familial AD (fAD (show PSEN1 Proteins)), does not.
amyloid and oxidative stress-related disease proteins like Alzheimer A beta (show SUCLA2 Proteins) peptide are increased in expression and form localized accumulations in diabetic muscle in this rabbit model of diabetes.
study suggests that hypercholesterolemia-induced Abeta accumulation may be mediated by 27-hydroxycholesterol, involving IGF-1 (show IGF1 Proteins) signaling
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.
alzheimer disease amyloid protein
, amyloid beta A4 protein
, beta-amyloid peptide
, cerebral vascular amyloid peptide
, peptidase nexin-II
, protease nexin-II
, amyloid protein
, alzheimer disease amyloid A4 protein homolog
, amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease)
, Amyloid beta A4 protein precursor (APP) (ABPP) (Alzheimers disease amyloid protein) (Cerebral vascular amyloid peptide) (CVAP) (Protease nexin-II) (PN-II) (APPI) (PreA4)
, amyloid beta (A4) precursor protein (peptidase nexin-2, Alzheimer disease)
, amyloid beta (A4) precursor protein (protease nexin-II, Alzheimer disease)
, beta-amyloid precursor protein
, amyloid precursor protein
, amyloid precursor protein-like
, amyloid A4
, amyloidogenic glycoprotein
, protease nexin II
, amyloid beta precursor protein a
, beta-amyloid precursor protein A