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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
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
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
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
Overexpression of SNX7 (show SNX7 ELISA Kits) in HEK293T cells reduces the levels of secreted Abeta and beta-cleaved N-terminal APP fragments (sAPPbeta). Moreover, SNX7 (show SNX7 ELISA Kits) overexpression caused a significant reduction of the steady-state levels of APP as well as of the cell surface APP levels.
modulation of proteostasis is a distinct biological function of sAPPalpha and does not require surface-bound holo-APP.
elevated levels of plasma homocysteine /homocysteine thiolactone contribute to AD pathology via the Abeta-fibrin(ogen) interaction
Overexpression of human APP in mice reduce cortical free cholesterol under normal diet and HFD.
The authors show that APP can physically interact with KCC2 (show SLC12A5 ELISA Kits), a neuron-specific K(+)-Cl(-) cotransporter (show SLC12A4 ELISA Kits) that is essential for Cl(-) homeostasis and fast GABAergic inhibition.
beta-amyloid interacts with fibrinogen and factor XII (show F12 ELISA Kits). These interactions can lead to increased clotting, abnormal clot (show TXNDC17 ELISA Kits) formation, persistent fibrin deposition, and generation of proinflammatory molecules.
Abeta activates FXII (show F12 ELISA Kits), resulting in FXI (show F11 ELISA Kits) activation and thrombin (show F2 ELISA Kits) generation in human plasma, thereby establishing Abeta as a possible driver of prothrombotic states
Data suggest that aggregates of amyloid beta(1-40) induce excessive generation of reactive oxygen species, MAPK (show MAPK1 ELISA Kits)/NFkappaB (show NFKB1 ELISA Kits) signaling activation, and NLRP3 (show NLRP3 ELISA Kits) inflammasome activation in retinal pigment epithelial cells mimicking changes seen in age-related macular degeneration; this mechanism is dependent on NADPH oxidase (show NOX1 ELISA Kits).
These results demonstrate a stage-dependent plasma Abeta increase that is augmented by loss of glomerulotubular integrity, low body weight, and inflammation, demonstrating a multifaceted role of renal dysfunction in Abeta retention.
Combining a murine APP-deficient and a human APP-transgenic strain, we were able to analyse the progression of the cortical amyloidosis independent of the murine variant. The lack of endogenous mAPP (show XPNPEP2 ELISA Kits) resulted in accelerated deposition and, thus, increased number of senile plaques and higher levels of aggregated hAbeta.
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 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.
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 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
Taken together, these results suggest that apoE (show APOE ELISA Kits)-containing discoidal HDLs (show CSF1R ELISA Kits) do not require LCAT (show LCAT ELISA Kits)-dependent maturation to mediate efficient Abeta clearance
APP knockout mice have shorter dendritic arbors in the hippocampus.
This study demonstrates the neuroprotective effect of TSG (show TWSG1 ELISA Kits) on APP expression, suggesting that TSG (show TWSG1 ELISA Kits) may be beneficial for AD prevention and treatment.
SNX15 (show SNX15 ELISA Kits) regulates the recycling of APP to cell surface and, thus, its processing for Abeta generation.
Immunohistochemical analysis confirmed increased amount of NOS1 (show NOS1 ELISA Kits) protein in neuronal somata and processes in the perilesional cortex in APP/PS1 (show PSEN1 ELISA Kits)-severe traumatic brain injury(TBI) mice compared to APP/PS1 (show PSEN1 ELISA Kits)-sham (p < 0.05) or Wt-sTBI mice (p < 0.01).
our findings indicate that sortilin (show SORT1 ELISA Kits) is a beneficial protein for the reduction of amyloid pathology in APP/PS1 (show PSEN1 ELISA Kits) mice by promoting APP degradation
APP levels then decrease progressively as a function of age in close relationship with the gradual normalization of FMRP and hnRNP C levels.
a 99-aa C-terminal fragment of APP,C99, in addition to its localization in endosomes, can also be found in mitochondria-associated endoplasmic reticulum (ER) membranes, where it is normally processed rapidly by gamma-secretase.
The authors concluded that the FcgammaRIIb-SHIP2 (show INPPL1 ELISA Kits) axis links Abeta neurotoxicity to tau pathology by dysregulating phosphoinositide metabolism, providing insight into therapeutic potential against Alzheimer's disease.
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.
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 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.
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