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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 - 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
Show all 4 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
Show all 3 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
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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
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
Human Polyclonal APP Primary Antibody for IC, IF - ABIN2451922
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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The neuronal specific alpha3 (alpha3)-subunit of the plasma membrane enzyme Na, K-ATPase (NKA) is a new binding partner of sAPPalpha.
Aggregation processes of ABETA on living cells and cytotoxic events were monitored by fluorescence techniques. ABETA formed amyloids after forming oligomers composed of approximately 10 ABETA molecules. The formation of amyloids was necessary to activate apoptotic caspase-3 and reduce the ability of the cell to proliferate; this indicated that amyloid formation is a key event in ABETA-induced cytotoxicity.
esults suggest that P-gp plays important role in mediating rivastigmine non-cholinergic beneficial effects, including Abeta brain load reduction, neuroprotective and anti-inflammatory effects in the AD mouse models.
Immature intracellular aggregates are more toxic than mature fibrillar ABETA(1-42).
Downregulation of C9orf72 in non-neuronal human cells overexpressing amyloid-beta protein precursor (AbetaPP) resulted in increased levels of secreted AbetaPP fragments and Abeta, while levels of AbetaPP or its C-terminal fragments (CTFs) remained unchanged. In neuronal cells, AbetaPP and C83 CTF levels were decreased upon C9orf72 knockdown, but those of secreted AbetaPP fragments or Abeta remained unchanged.
N-terminal mutations can affect Abeta fibril and oligomer formation, despite lying outside the core amyloid region of Abeta. Of the three factors that may influence Abeta-mediated toxicity (primary structure of Abeta, assembly structure and cellular responses), results suggest that it is more the assembly structure that correlates with effects on cell viability.
The Swedish variant was a more potent co-activator of Wnt-PCP signalling than wild-type APP and, unlike wild-type APP, which co-activates Wnt beta-catenin signalling, APPSwe suppressed this branch of Wnt.
Among hip fracture patients, 88.6% of the cognitively normal (Clinical Dementia Rating-CDR 0; n = 70) and 98.8% with mild cognitive impairment (CDR 0.5; n = 81) fell in the abnormal biomarker categories by CSF Abeta42/40 ratio, p-tau, and t-tau measures.
FNDC5 significantly affects beta-cleavage of APP via the interaction with APP.
uncovered for the first time a phenomenon of chaperone antagonism on BACE1-mediated Abeta42 generation.
This study investigated the assembly mechanisms of dimeric ABETA 16-22 and found that the fibril formation rate is predominantly controlled by the total beta-strand content.
Data suggest that the substitution of alanine by valine at position 2 of the amyloidogenic peptide affect the lateral interactions between fibrils, promoting a more compact, aligned and uniform structure which explains its aggressiveness in homozygous carriers and its prophylactic effect in heterozygous carriers.
Solution NMR allowed us to define the secondary structure of this Abeta dimer, which shows interlocking contacts between C-terminal peptide strands. Thus, we present a novel Abeta oligomer that resists conversion to fibrils and remains stable for more than one year.
Data suggest that antiinflammatory agents, non steroidal (NSAIDs) bind to amyloid beta (Abeta) protein leading to the blockage of hydrophobic site which might prevent incoming Abeta molecules from extending the fibril.
Findings suggest that the polymorphisms of amyloid-beta (Abeta) fibril structures are caused by differences in the surrounding ionic environment.
Young healthy adults carrying APOE epsilon4 and APP/presenilin-1/2 displayed different hippocampus functional connectivity patterns
X-box binding protein 1 overexpression at an early stage reversed Abeta-induced early death without affecting learning performance in the Abeta42 transgenic flies. PERK activation was determined to only enhance Abeta-induced learning deficits.
data suggests that the hydrophobic interactions between beta-casein and Abeta1-42 play an important role in the burial of the hydrophobic part of the Abeta1-42.
APP-Knockout astrocytes have reduced cholesterol and elevated levels of sterol regulatory element-binding protein (SREBP) target gene transcripts and proteins, which were both downstream consequences of reduced lipoprotein endocytosis.
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
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
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.
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.
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