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Human Polyclonal APP Primary Antibody for IHC (p), WB - ABIN3044384
Li, Li, Huang, Kan, Wang, Wu, Yin, Yao: Dexamethasone and A???-?? accelerate learning and memory impairments due to elevate amyloid precursor protein expression and neuronal apoptosis in 12-month male rats. in Behavioural brain research 2011
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Human Polyclonal APP Primary Antibody for IHC (p), WB - ABIN965581
Duce, Tsatsanis, Cater, James, Robb, Wikhe, Leong, Perez, Johanssen, Greenough, Cho, Galatis, Moir, Masters, McLean, Tanzi, Cappai, Barnham, Ciccotosto, Rogers, Bush: Iron-export ferroxidase activity of β-amyloid precursor protein is inhibited by zinc in Alzheimer's disease. in Cell 2010
Show all 4 Pubmed References
Human Polyclonal APP Primary Antibody for IC, IF - ABIN2451920
Kang, Lemaire, Unterbeck, Salbaum, Masters, Grzeschik, Multhaup, Beyreuther, Müller-Hill: The precursor of Alzheimer's disease amyloid A4 protein resembles a cell-surface receptor. in Nature 1987
Show all 5 Pubmed References
Human Polyclonal APP Primary Antibody for IHC (p), WB - ABIN3043787
Qin, Yao, Huang: Effects of compound danshen tablets on spatial cognition and expression of brain beta-amyloid precursor protein in a rat model of Alzheimer's disease. in Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan / sponsored by All-China Association of Traditional Chinese Medicine, Academy of Traditional Chinese Medicine 2012
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Human Polyclonal APP Primary Antibody for IC, IF - ABIN2451919
Selkoe: Normal and abnormal biology of the beta-amyloid precursor protein. in Annual review of neuroscience 1994
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Human Polyclonal APP Primary Antibody for IC, IF - ABIN2451921
Nishimura, Uetsuki, Kuwako, Hara, Kawakami, Aimoto, Yoshikawa: Cell death induced by a caspase-cleaved transmembrane fragment of the Alzheimer amyloid precursor protein. in Cell death and differentiation 2002
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Human Polyclonal APP Primary Antibody for IC, IF - ABIN2451922
Nishimura, Takazaki, Kuwako, Enokido, Yoshikawa: Upregulation and antiapoptotic role of endogenous Alzheimer amyloid precursor protein in dorsal root ganglion neurons. in Experimental cell research 2003
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Human Polyclonal APP Primary Antibody for ELISA, WB - ABIN545822
Lleó, Berezovska, Ramdya, Fukumoto, Raju, Shah, Hyman: Notch1 competes with the amyloid precursor protein for gamma-secretase and down-regulates presenilin-1 gene expression. in The Journal of biological chemistry 2003
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Human Polyclonal APP Primary Antibody for ELISA, WB - ABIN537558
Zhou, Su, Li, Liu, Ryder, Wu, Gonzalez-DeWhitt, Gelfanova, Hale, May, Paul, Ni: Nonsteroidal anti-inflammatory drugs can lower amyloidogenic Abeta42 by inhibiting Rho. in Science (New York, N.Y.) 2003
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Human Polyclonal APP Primary Antibody for ELISA, WB - ABIN545823
Borroni, Colciaghi, Caltagirone, Rozzini, Broglio, Cattabeni, Di Luca, Padovani: Platelet amyloid precursor protein abnormalities in mild cognitive impairment predict conversion to dementia of Alzheimer type: a 2-year follow-up study. in Archives of neurology 2003
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Identified TMEM30A as a candidate partner for beta-carboxyl-terminal fragment (betaCTF) of amyloid-beta precursor protein (APP). TMEM30A physically interacts with betaCTF in endosomes and may impair vesicular traffic, leading to abnormally enlarged endosomes. Data suggested that TMEM30A is involved in betaCTF-dependent endosome abnormalities that are related to Abeta overproduction
ASIC1a modulates the ABETA-mediated increase in intrinsic excitability of CA1 pyramidal neurons. The study was performed on APP transgenic mice (Tg2576) expressing high levels of human mutant (K670N/M671L) APP transgene (hAPPK670N/M671L).
For the first time, natural ABETA (1-42) fibrils (WT) implicated in Alzheimer's disease, as well as two synthetic mutants forming less toxic amyloid fibrils (L34T) and highly toxic oligomers (oG37C), are chemically characterized at the scale of a single structure using tip-enhanced Raman spectroscopy .
Male heterozygous (HET) APP23 mice, overexpressing human APP 751 carrying the Swedish double mutation (K670M/N671L) were used for all experiments. The ABETA 1-42/ABETA 1-40 ratio spikes at 2 distinct ages: 1.5 months and 18 months. An initial build up in APP, C-terminal fragment beta and ABETA is observed at a young age. An increase in ABETA 1-42 at 18 months is followed by an increase in ABETA 1-40.
This study shows by Atomic Force Microscopy that attachment of ApoE4/ABETA complexes to basement membrane laminin is significantly weaker than ApoE3/ABETA complexes.
The pattern of development of cerebral amyloid angiopathy in the human brain suggests expansion of ABETA from the basement membranes to progressively replace all tissue elements in the artery wall.
The purpose of this review article is to summarize recent research on how cerebral vascular ABETA and amyloid beta precursor protein influence cerebral hemostasis. [review]
genetic manipulation of Sirt3 revealed that amyloid-beta increased levels of total tau acetylated tau through its modulation of Sirt3.
brain. In the present study, two familial Ab42 mutations, namely A2V (harmful) and A2T (protective) have been analyzed and compared with the wild-type (WT) by performing all-atom molecular dynamics (MD) simulations in the absence and presence of curcumin, a well-known inhibitor of Abeta plaque formation. Mutant A2V was found to exhibit highest stability followed by WT and mutant A2T in the absence of curcumin
These results provide evidence for an emerging role of BAG-1M in the regulation of BACE1 expression and AD pathogenesis and that targeting the BAG-1M-NF-kappaB complex may provide a mechanism for inhibiting Abeta production and plaque formation.
A physical interaction between nicastrin (hNCT) and the gamma-secretase substrate amyloid beta-protein precursor (APPC100) confirmed the functionality of hNCT as a substrate recognizer.
ethanol-induced eIF2alpha phosphorylation stimulates COX-2 expression and PGE2 production which induces the BACE1 expression and Abeta production via EP-2 receptor-dependent PKA/CREB pathway.
Western diet (WD) dramatically increases ABETA levels and generates pyroglutamate-ABETA deposits.
This study demonstrated that the APP21 transgenic rats develop age-dependent cognitive impairment and accelerated white matter inflammation.
Data suggest that kinetics of degradation/proteolysis versus of aggregation of amyloid beta(1-40) and amyloid beta(1-42) at specific concentrations of amyloid beta, cathepsin B, and cystatin C can be modeled and predicted.
In vitro neuroprotective effects of naringenin nanoemulsion against beta-amyloid toxicity through the regulation of amyloidogenesis and tau phosphorylation.
The results of study demonstrate that different degradation pathways play distinct roles in the removal of Abeta42 aggregates and in disease progression. These findings also suggest that pharmacologic treatments that are designed to stimulate cellular degradation pathways in patients with AD should be used with caution.
This data demonstrates a specific function of APP or its metabolites is involved in the changes that occur during high fat diet-induced obesity.
Our study provides new insights into the regulation of APP pre-mRNA processing, supports the role for nELAVLs as neuron-specific splicing regulators and reveals a novel function of AUF1 in alternative splicing.
Data show that phospholipase D3 (PLD3) functions in endosomal protein sorting and plays an important role in regulating amyloid precursor protein (APP) processing.
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 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.
The results of this study showed that increased production of the endogenous Drosophila Amyloid Intracellular Domain (dAICD) caused disruption of circadian rest-activity rhythms during aging.
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-PCP pathway specifically required for axon outgrowth.
Data show that Appl is directly regulated by the Ras/MAPK pathway through a mechanism mediated by PntP2.
[review] APP-like proteins are involved in neuronal differentiation, neuritic outgrowth, and synapse formation.
Disruption of amyloid protein 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) reduces amyloid-beta production by altering Nicastrin maturation and intracellular localization.
accumulation of Ass42 plaques induces JNK signaling in neurons and induction of JNK contributes to Ass42 mediated cell death
Findings show that age-related changes in amyloid characteristics may be a trigger for late-onset polyglutamine diseases.
in adult flies, APPL is not required for learning but is specifically involved in long-term memory, a long lasting memory whose formation requires de novo protein synthesis and is thought to require synaptic structural plasticity.
Abeta42 levels were reduced upon GSK-3 inhibition, pointing to a direct role of GSK-3 in the regulation of Abeta42 peptide level, in the absence of APP processing.
Data suggest that toxic effects of amyloid beta-peptide aggregation in vivo can therefore be eliminated by sequestration of hydrophobic regions in monomeric peptides, even when these are extremely aggregation prone.
APP-Like (APPL) can induce postdevelopmental axonal arborization, which depends critically on a conserved motif in the C-terminus and requires interaction with the Abelson (Abl) tyrosine kinase.
Study shows that APP-BP1 specifically binds the intracellular domain of APP-like protein (APPL), APP-BP1 mutation partially suppresses the abnormal macrochaete phenotype of Appl(d), while overexpression of dAPP-BP1 causes abnormal macrochaetes.
These data offer insight into the toxicity of Abeta and open new areas for further study into Alzheimer's disease pathogenesis.
findings show that Abeta fragments aggregate into intracellular fibrils, amyloid deposits, and cause age-dependent behavioral deficits and neurodegeneration
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
APPsw mutation for Alzheimer's disease is not associated with object recognition.
Amyloid-beta inhibits No-cGMP signaling in a CD36- and CD47-dependent manner
These experiments demonstrate the roles of Chol and ApoE 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 uncovered two clear phases in the life of APP23 mice: developmental and aging. Development displays similarities to young carriers of familial Alzheimer's disease (AD) mutations. All gene expression differences between APP23 and control mice correlate with aging. Age-related expression changes appear exacerbated/accelerated in APP23 mice.
Conformational changes in a mouse model of Alzheimer's disease-linked amyloid beta and APP take place before the amyloids plaques can be seen.
These results support the proposition that Aβ release during thrombosis serves as part of a natural defense against infection.
These data suggest a novel regulatory function of juxta- and intra-membrane domains on the metabolism and function of APP.
Inflammasome-derived cytokine IL18 suppresses amyloid-induced seizures in Alzheimer-prone mice.
pharmacological inhibition of PARP-1 reversed both particulate matter-induced Abeta increase and glial activation.
The concentrations of Abeta (1-42) were also significantly higher in early stage Alzheimer's disease (AD) mice compared with WT mice, however, the levels were markedly lower compared with later stage AD mice, as determined by ELISA. In addition to increased levels of Abeta (1-42) in mice with later stage AD, reduced astrocyte staining was observed compared with WT mice.
work expands the current knowledge regarding Abeta seeding and the consequences thereof and attributes microglia an important role in diminishing Abeta seeding by environmental enrichment.
This study demonstrated that APP as a novel receptor for Slit ligand mediating axon guidance and neural circuit formation.
In vivo, the NHE6 knockout (NHE6(KO)) mouse model showed elevated Abeta in the brain, consistent with a causal effect. Increased nuclear translocation of histone deacetylase 4 (HDAC4) in ApoE4 astrocytes, compared with the nonpathogenic ApoE3 allele, suggested a mechanistic basis for transcriptional down-regulation of NHE6.
This commentary reviews the role of the Alzheimer amyloid peptide Abeta on basal synaptic transmission, synaptic short-term plasticity, as well as short- and long-term potentiation in transgenic mice, with a special focus on N-terminal truncated Abeta4-42.
ADAP KO mice developed glomerular pathology. ADAP KO podocytes lack cell protrusions with actin cytoskeleton forming circumferential stress fibers.
Therefore, APP modulates Nav1.6 sodium channels through a Go-coupled JNK pathway, which is dependent on phosphorylation of APP at Thr668.
These findings suggest that in the absence of CLU, Abeta clearance shifts to perivascular drainage pathways, resulting in fewer parenchymal plaques but more CAA because of loss of CLU chaperone activity, complicating the potential therapeutic targeting of CLU for AD.
Chronic Dyrk1 inhibition reversed cognitive deficits in Alzheimer's disease transgenic mice via reduction of APP and phosphorylated tau pathology.
The findings provide a model for initiation of synaptic dysfunction whereby exposure to physiologic levels of amyloid beta for a prolonged period of time causes microstructural changes at the synapse which result in increased transmitter release, failure of synaptic plasticity, and memory loss.
The results of the present study substantiate that cGMP has a role in the endocytic pathway of APP and suggest a scenario where the cyclic nucleotide enhances the production of Abeta by favoring the trafficking of APP from the cell cortex to the endolysosomal compartment.
Study showed that the APP Osaka mutation has dual effects: it causes a loss-of-function of APP and gain-of-toxic-function of Abeta, though the latter seems to come out only after the former causes GABAergic depletion. Also present OSK-KI mice as a mouse model to replicate the hereditary form of recessive familial Alzheimer's disease.
Enhancing mitochondrial proteostasis reduces amyloid-beta proteotoxicity
Amyloid beta precursor protein and prion protein 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 and Aplp2 fusion proteins are likely secreted from the central nervous system and accumulate in the embryonic veins independent of blood flow.
expression pattern during embryonic development
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), 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" 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 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 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