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Human APP ELISA Kit for Sandwich ELISA - ABIN414520
Shi, Wu, Xu, Zou: Bilobalide regulates soluble amyloid precursor protein release via phosphatidyl inositol 3 kinase-dependent pathway. in Neurochemistry international 2011
Show all 2 Pubmed References
Human APP ELISA Kit for Sandwich ELISA - ABIN921082
Turner, OConnor, Tate, Abraham: Roles of amyloid precursor protein and its fragments in regulating neural activity, plasticity and memory. in Progress in neurobiology 2003
Show all 3 Pubmed References
Rat (Rattus) APP ELISA Kit for Sandwich ELISA - ABIN810848
Tian, Guo, Yue, Lv, Ye, Wang, Chen, Wu, Xu, Liu: Intranasal administration of nerve growth factor ameliorate ?-amyloid deposition after traumatic brain injury in rats. in Brain research 2012
Rat (Rattus) APP ELISA Kit for Sandwich ELISA - ABIN579070
Grolla, Fakhfouri, Balzaretti, Marcello, Gardoni, Canonico, DiLuca, Genazzani, Lim: Aβ leads to Ca²⁺ signaling alterations and transcriptional changes in glial cells. in Neurobiology of aging 2012
Mouse (Murine) APP ELISA Kit - ABIN1882413
Zhang, Hu, Teng, Tang, Chen: Synaptic and cognitive improvements by inhibition of 2-AG metabolism are through upregulation of microRNA-188-3p in a mouse model of Alzheimer's disease. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2014
Human APP ELISA Kit - ABIN1882410
Qosa, Abuasal, Romero, Weksler, Couraud, Keller, Kaddoumi: Differences in amyloid-? clearance across mouse and human blood-brain barrier models: kinetic analysis and mechanistic modeling. in Neuropharmacology 2014
Appl siRNA inhibition in cortex glia resulted in longer sleep and reduced expression of genes involved in glutamate (show GRIN2A ELISA Kits) 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 ELISA Kits)-PCP (show PRCP ELISA Kits) pathway specifically required for axon outgrowth.
Data show that Appl is directly regulated by the Ras/MAPK (show MAPK1 ELISA Kits) pathway through a mechanism mediated by PntP2 (show ETS2 ELISA Kits).
[review] APP-like proteins are involved in neuronal differentiation, neuritic outgrowth, and synapse formation.
Disruption of amyloid protein (show IAPP ELISA Kits) 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 ELISA Kits)) reduces amyloid-beta production by altering Nicastrin (show NCSTN ELISA Kits) maturation and intracellular localization.
accumulation of Ass42 plaques induces JNK (show MAPK8 ELISA Kits) signaling in neurons and induction of JNK (show MAPK8 ELISA Kits) contributes to Ass42 mediated cell death
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 ELISA Kits) isoforms, suggests that the significance of arginases for the promotion of NOS (show NOS1 ELISA Kits)-dependent cellular stress by betaAPP/Abeta in a system where up-regulated, potentially pathogenic miRNAs are involved.
Compared with noncarriers, carriers of the APPswe mutation have significantly decreased CSF (show CSF2 ELISA Kits) levels of sAPPalpha and Abeta42 whereas the levels of Abeta38 and Abeta40 were not significantly different.
Data suggest that single aromatic/hydrophobic amino acid residues within IAPP (islet amyloid polypeptide (show IAPP ELISA Kits)) amyloid core region are able to control its interaction with amyloid-beta(1-40) or amyloid-beta(1-42) but not IAPP (show IAPP ELISA Kits) self-assembly; four aromatic/hydrophobic residues are able to control both IAPP (show IAPP ELISA Kits) amyloid self-assembly and its cross-interaction with amyloid-beta(1-40) or amyloid-beta(1-42).
The search for the genetic factors contributing to Alzheimer disease (AD) has evolved tremendously throughout the years. It started from the discovery of fully penetrant mutations in Amyloid precursor protein, Presenilin 1 (show PSEN1 ELISA Kits), and Presenilin 2 (show PSEN2 ELISA Kits) as a cause of autosomal dominant AD
The authors now show that the very little Abeta generated by PS1 (show PSEN1 ELISA Kits) L435F mutant consists primarily of Abeta43, a highly amyloidogenic species which was overlooked in previous studies of this mutant.
Complicated function of dopamine in Abeta-related neurotoxicity: Dual interactions with Tyr (show TYR ELISA Kits)(10) and SNK (show ATP1A4 ELISA Kits)(26-28) of Abeta
These studies support the hypothesis that the ratio of Abeta monomers to Abeta oligomers is a critical factor that regulates synapse damage.
UBQLN4, APP, CTNNB1 (show CTNNB1 ELISA Kits), SHBG (show SHBG ELISA Kits), and COL1A1 (show COL1A1 ELISA Kits) might be involved in the development of nonalcoholic fatty liver disease, and are proposed as the potential markers for predicting the development of this condition
Fe65 (show APBB1 ELISA Kits) is an adaptor protein involved in both processing and signaling of the Alzheimer-associated amyloid-beta precursor protein, APP. Here, the subcellular localization was further investigated using TAP-tagged Fe65 (show APBB1 ELISA Kits) constructs expressed in human neuroblastoma (show ARHGEF16 ELISA Kits) cells. Our results indicate that PTB2 (show PTBP1 ELISA Kits) rather than the WW domain (show DRP2 ELISA Kits) is important for the nuclear localization of Fe65 (show APBB1 ELISA Kits).
bis (show BAG3 ELISA Kits)(sulfosuccinimidyl) suberate (BS3) was used to cross-link Abeta1-42 oligomers prior to electrophoresis. When compared to a previously reported Abeta cross-linking agent, glutaraldehyde, it was quite apparent that BS3 is more suitable for detecting intra-membrane Abeta oligomers and extra-membrane Abeta oligomers states.
Amyloid-beta inhibits No-cGMP signaling in a CD36 (show CD36 ELISA Kits)- and CD47 (show CD47 ELISA Kits)-dependent manner
These experiments demonstrate the roles of Chol and ApoE (show APOE ELISA Kits) 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
results suggest that PrP(C (show PRNP ELISA Kits)) 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 ELISA Kits) to trigger necroptosis, and targeting DR6 (show TNFRSF21 ELISA Kits)-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 ELISA Kits)-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 ELISA Kits) signaling pathway which is involved in the regulation of Abeta1-42 internalization in the parietal cortex and hippocampus of mouse through LRP1 (show LRP1 ELISA Kits) in vivo.
increased APP and/or beta-CTF (show NFIA ELISA Kits) impact the endocytic pathway to disrupt NGF (show NGFB ELISA Kits) trafficking and signaling, resulting in trophic deficits in basal forebrain cholinergic neurons.
ABETA 25-35 downregulated miR (show MLXIP ELISA Kits)-137 and upregulated TNFAIP1 (show TNFAIP1 ELISA Kits) in cortical neurons and N2a cells.
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 ELISA Kits)" 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 ELISA Kits) 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 ELISA Kits) and Aplp2 (show APLP2 ELISA Kits) 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 ELISA Kits)), does not.
amyloid and oxidative stress-related disease proteins like Alzheimer A beta (show SUCLA2 ELISA Kits) 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 ELISA Kits) 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.
, amyloid precursor protein
, amyloid precursor protein-like
, amyloid beta (A4) precursor protein
, amyloid beta A4 protein
, amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease)
, amyloid beta (A4) precursor protein (peptidase nexin-2, Alzheimer disease)
, amyloid beta (A4) precursor protein (protease nexin-II, Alzheimer disease)
, beta-amyloid precursor protein
, alzheimer disease amyloid protein
, beta-amyloid peptide
, cerebral vascular amyloid peptide
, peptidase nexin-II
, protease nexin-II
, amyloid protein
, alzheimer disease amyloid A4 protein homolog
, amyloidogenic glycoprotein
, protease nexin II
, amyloid A4
, beta-amyloid precursor protein A
, 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 precursor protein a