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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
The amyloid hypothesis proposes that Alzheimer's Disease is caused by altered beta-amyloid precursor protein expression or APP-mutation-induced Ab aggregation, following an imbalance between Ab production and Ab clearance.
Phosphorylation of amyloid precursor protein by mutant LRRK2 promotes AICD activity and neurotoxicity in Parkinson's disease.
Mass spectrometry analysis of APP intracellular domains revealed differential processing of APP-C83, APP-C89, and APP-C99 by gamma-secretase already at the epsilon-cleavage stage. This mechanistic insight could aid in developing substrate-targeted modulators of APP-C99 processing to specifically lower the Abeta42:Abeta40 ratio without compromising gamma-secretase function.
enzymes known to act in other metabolic pathways, such as meprin beta (show MEP1B Proteins), have been found to cleave APP to yield products known to participate in AD pathologies. This review provides an overview of current knowledge of conventional and novel APP processing.
study provides molecular insights into the design of amyloidogenic inhibitors to cure various neurodegenerative and amyloid-associated diseases, as NABi would regulate aggregation of other toxic beta-sheet proteins other than Abeta.
Remarkably, the cyclic neuroendocrine peptide somatostatin-14 (show SST Proteins) (SST14) was observed to be the most selectively enriched oligomeric Abeta1-42 binder.
This is the first evidence of cortical calcification in patients with an APP mutation other than the Iowa mutation.
Abeta*56 activated Ca(2+)-dependent calmodulin kinase II and increased site-specific phosphorylation and missorting of tau, both of which are associated with Alzheimer's disease pathology.
data point to a scenario where neuroinflammatory processes together with direct synaptotoxic effects are caused by posttranslational modification of soluble oligomeric Abeta and contribute synergistically to the onset of synaptic dysfunction in Alzheimer's disease
xplored structural details of fibrils formed by a mutated amyloid beta (Abeta(1-40)) peptide carrying a Phe19 to Lys19 mutation. Although morphologically very robust, local perturbations of the Abeta(1-40) sequence lead to moderate structural alterations with tremendous impact on the physiological importance of these aggregates, which may suggest alternative strategies for the development of a remedy against Alzheimer'...
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.
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
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
Data show that exosomal amyloid precursor protein C-terminal fragments (APP-CTFs) and bis(monoacylglycero)phosphate (BMP) as candidate biomarkers diagnostic of endolysosomal dysfunction associated with neurodegenerative disorders.
Conducted in vivo extracellular recording to investigate cholinergic compound action potentials of the superior cervical ganglion (SCG (show KPNB1 Proteins)) in APP(-/-) and littermate wild-type (WT) mice; found that APP not only regulates presynaptic activity, but also affects postsynaptic function at cholinergic synapses in SCG (show KPNB1 Proteins); also alpha4beta2 and alpha7 nicotinic acetylcholine receptors are reduced in the absence of APP.
App-KI mouse lines with different levels of pathophysiology are useful models of AD.
Loss of Abpp is associated with cognitive impairment.
long term survival and amyloid protein (show IAPP Proteins) levels are modified by positive and negative early life experiences in a mouse model of Alzheimer's disease
the synaptic localization of APP, ADAM10 (show ADAM10 Proteins), and BACE1 (show BACE Proteins) in the mouse cerebral cortex, was examined.
Taken together, these results suggest that apoE (show APOE Proteins)-containing discoidal HDLs (show CSF1R Proteins) do not require LCAT (show LCAT Proteins)-dependent maturation to mediate efficient Abeta clearance
APP knockout mice have shorter dendritic arbors in the hippocampus.
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.
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 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