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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
Show all 9 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
Show all 4 Pubmed References
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 ELISA, WB - ABIN537558
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
Show all 3 Pubmed References
Human Polyclonal APP Primary Antibody for ELISA, WB - ABIN545822
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
Show all 3 Pubmed References
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
Show all 3 Pubmed References
Mouse (Murine) Polyclonal APP Primary Antibody for IHC (fro) - ABIN542621
Wilson, Doms, Lee: Distinct presenilin-dependent and presenilin-independent gamma-secretases are responsible for total cellular Abeta production. in Journal of neuroscience research 2003
Show all 3 Pubmed References
Dog (Canine) Polyclonal APP Primary Antibody for WB - ABIN550153
Liu, Su, Li, Zhou, Ryder, Gonzalez-DeWhitt, May, Ni: Regulation of amyloid precursor protein (APP) phosphorylation and processing by p35/Cdk5 and p25/Cdk5. in FEBS letters 2003
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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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The findings reveal a novel mechanism whereby GSK3beta stimulates amyloidogenic processing of APP by phosphorylation of FE65 at threonine 579.
A Toxic Conformer of Abeta42 with a Turn at 22-23 is a Novel Therapeutic Target for Alzheimer's Disease.
Alzheimer's disease-associated TREM2 variants bind Abeta with equivalent affinity but show loss of function in terms of signaling and Abeta internalization.
PKCdelta knockdown reduces BACE1 expression, BACE1-mediated APP processing, and Abeta production.
recombination of APP in human neurons, occurring mosaically as thousands of variant 'genomic cDNAs' (gencDNAs); gencDNAs lacked introns and ranged from full-length cDNA copies of expressed, brain-specific RNA splice variants to myriad smaller forms that contained intra-exonic junctions, insertions, deletions, and/or single nucleotide variations
results confirm the presence of Abeta seeds in archived c-hGH vials and are consistent with the hypothesized iatrogenic human transmission of Abeta pathology; this experimental confirmation has implications for both the prevention and the treatment of Alzheimer's disease, and prompt a review of the risk of iatrogenic transmission of Abeta seeds by medical and surgical procedures long recognized to pose a risk of prion ...
Fpn and Heph co-localize, and FRET analysis indicated that the two proteins form an iron-efflux complex; in contrast, none of the full-length, cellular APP proteins exhibited Fpn co-localization or FRET
we show that F-actin depolymerization in spines leads to a breakdown of the nano-organization of outwardly radiating F-actin rods in cortical neurons from APPswe/PS1DeltaE9 mice
It was evident that on average only a single histidine residue coordinates Cu(II) in monomeric ABETA(1-42) at pH 6.1, in addition to 3 other oxygen or nitrogen ligands. Cu(II) coordination in ABETA(1-42) at pH 7.4 is similarly 4-coordinate with oxygen and nitrogen ligands, although an average of 2 histidine residues appear to coordinate at this pH.
High carboxypeptidase A4 (CPA4) expression in triplenegative breast cancer (TNBC) cases is associated with low expression of E-cadherin and with the expression of cancer stem cell markers. Patients with TNBC and high levels of CPA4 expression have poorer prognosis compared with those with low CPA4 expression. Viability and migration are reduced, but E-cadherin expression is upregulated in CPA4-suppressed TNBC cells.
Overexpression of AbetaPP in Muller cells (MC) induced strong antioxidant and anti-ER stress (PERK downregulation and GADD34 upregulation) responses accompanied by activation of the prosurvival branch of the unfolded protein response. It was also associated with upregulation of major genes involved in MC-controlled retinal homeostasis (KCNJ10, GS, and RLBP1) and protection against HNE-induced apoptosis.
plasma amyloid beta protein level may predicti cognitive decline in patients suffering from chronic kidney disease.
BIN1 rs744373 SNP is associated with increased tau but not beta-amyloid pathology, suggesting that alterations in BIN1 may contribute to memory deficits via increased tau pathology
the presence of ApoEepsilon4 allele might also have a possible effect on the amyloid beta phagocytosis efficiency of the macrophages.
Using Western blotting, kinetic assays, and microfluidic analyses, the study shows that FXIIIa covalently cross-links ABETA40 into dimers and oligomers (k cat/Km = 1.5 x 10(5) m(-1)s(-1)), as well as to fibrin, platelet proteins, and blood clots under flow in vitro ABETA40 also increased the stiffness of platelet-rich plasma clots in the presence of FXIIIa.
As indicated by a comparison between experiment and computation, the number of adjacent beta-strands per peptide molecule is two for ABETA40 oligomers and two or more for ABETA42 oligomers. These results are well explained by regular, antiparallel beta-sheets or beta-barrels.
Study shows attenuated pain-like behaviour in a transgenic mouse model of Alzheimer's disease (bearing mutant human amyloid precursor protein (APP) (695-aa isoform)) due to alterations in the opioidergic system and central plasticity mechanisms of persistent pain.
The primary conclusion is that, under copper-limiting conditions, the M1 site in domain E2 dominates the properties of the entire APP ectodomain with comparable picomolar affinities for both oxidation states Cu(I) and Cu(II).
These results demonstrated the contributory role of APP cleavage on its oncogenic roles in breast cancer. ADAM10 was the key alpha-secretase. APP and ADAM10 co-expression was associated with worse survival in non-luminal breast cancers.
The neuronal specific alpha3 (alpha3)-subunit of the plasma membrane enzyme Na, K-ATPase (NKA) is a new binding partner of sAPPalpha.
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
NRBF2 plays an important role in regulating degradation of APP-C-terminal fragments through modulating autophagy.
These results provide evidence that both central circadian rhythms and local clock function influence Abeta dynamics and plaque formation.
These data identified APP and APLP2 as modulators of normal myelination and demyelination/remyelination conditions.
these findings suggest that endogenous Abeta is involved in memory forgetting in the normal brain.
pterostilbene attenuated the neuroinflammatory response induced by Abeta1-42 in microglia through inhibiting the NLRP3/caspase-1 inflammasome pathway, indicating that pterostilbene might be an effective therapy for AD.
Abeta40 and Abeta42 demonstrated distinct distribution kinetics in plasma and brain compartments, and insulin differentially modulated their distribution.
APP/GBR complex formation links presynaptic GBR trafficking to Abeta formation.
APP knockout increases synaptic GluA1, PSD-95 and synaptophysin expression and reduces drebrin expression.
data indicate that Drp1 is a direct target of Cdk5, and Cdk5-mediated phosphorylation of Drp1 at Serine 579 regulates Abeta1-42 induced mitochondrial fission and neuronal toxicity.
miR98 reduced the production of Abeta and improved oxidative stress and mitochondrial dysfunction through activation of the Notch signaling pathway by binding to HEY2 in Alzheimer's disease mice.
Heme and Hb suppress immune activity of primary mouse astrocytes by reducing expression of several proinflammatory cytokines (e.g. RANTES (regulated on activation normal T cell expressed and secreted)) and the scavenger receptor CD36 and reducing internalization of Abeta(1-42) by astrocytes.
extracellular cholesterol concentration in serum under conditions of Npc1 deficiency can influence intracellular cholesterol content/distribution and lysosomal efficacy, triggering the accumulation of toxic APP-cleaved products, eventually leading to cell death.
Hippocampal mutant APP and amyloid beta-induced cognitive decline, dendritic spine loss, defective autophagy, mitophagy and mitochondrial abnormalities in a mouse model of Alzheimer's disease.
This study provides a novel mechanism underlying aggregation of Abeta peptides via BC1 induction of APP mRNA translation.
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.
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.
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.
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