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Abeta encodes a cell surface receptor and transmembrane precursor protein that is cleaved by secretases to form a number of peptides. Zusätzlich bieten wir Ihnen beta Amyloid Antikörper (277) und und viele weitere Produktgruppen zu diesem Protein an.
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The authors show that APP (zeige APP ELISA Kits) can physically interact with KCC2 (zeige SLC12A5 ELISA Kits), a neuron-specific K(+)-Cl(-) cotransporter (zeige SLC12A4 ELISA Kits) that is essential for Cl(-) homeostasis and fast GABAergic inhibition.
beta-amyloid interacts with fibrinogen and factor XII (zeige F12 ELISA Kits). These interactions can lead to increased clotting, abnormal clot (zeige TXNDC17 ELISA Kits) formation, persistent fibrin deposition, and generation of proinflammatory molecules.
Abeta (zeige APP ELISA Kits) activates FXII (zeige F12 ELISA Kits), resulting in FXI (zeige F11 ELISA Kits) activation and thrombin (zeige F2 ELISA Kits) generation in human plasma, thereby establishing Abeta (zeige APP ELISA Kits) as a possible driver of prothrombotic states
Data suggest that aggregates of amyloid beta(1-40) induce excessive generation of reactive oxygen species, MAPK (zeige MAPK1 ELISA Kits)/NFkappaB (zeige NFKB1 ELISA Kits) signaling activation, and NLRP3 (zeige 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 (zeige NOX1 ELISA Kits).
These results demonstrate a stage-dependent plasma Abeta (zeige APP ELISA Kits) increase that is augmented by loss of glomerulotubular integrity, low body weight, and inflammation, demonstrating a multifaceted role of renal dysfunction in Abeta (zeige APP ELISA Kits) retention.
Combining a murine APP (zeige APP ELISA Kits)-deficient and a human APP (zeige APP ELISA Kits)-transgenic strain, we were able to analyse the progression of the cortical amyloidosis independent of the murine variant. The lack of endogenous mAPP (zeige XPNPEP2 ELISA Kits) resulted in accelerated deposition and, thus, increased number of senile plaques and higher levels of aggregated hAbeta.
APP levels then decrease progressively as a function of age in close relationship with the gradual normalization of FMRP and hnRNP C levels.
In Alzheimer's Disease brain, amyloid Beta-protein binds to synapses and requires the expression of amyloid precursor protein (zeige APP ELISA Kits) to disrupt synaptic activity.
activation of mTOR (zeige FRAP1 ELISA Kits) signalling via RHEB (zeige RHEB ELISA Kits) over-expression inhibited the starvation-induced autophagy but did not affect trafficking of tf-Amyloid precursor protein (APP (zeige APP ELISA Kits)). These results show tf-APP (zeige APP ELISA Kits) can be used to determine how APP (zeige APP ELISA Kits) is trafficked through the lysosomal system of the cell.
Study found that FERMT2 (zeige FERMT2 ELISA Kits) (a beta3-integrin (zeige ITGB3 ELISA Kits) co-activator) was significantly associated with a variation in cerebrospinal fluid Abeta (zeige APP ELISA Kits) peptide levels in 2886 Alzheimer's disease cases.Under-expression of FERMT2 (zeige FERMT2 ELISA Kits) increases Abeta (zeige APP ELISA Kits) peptide production by raising levels of mature APP (zeige APP ELISA Kits) at the cell surface and facilitating its recycling
This study demonstrates the neuroprotective effect of TSG (zeige TWSG1 ELISA Kits) on APP (zeige APP ELISA Kits) expression, suggesting that TSG (zeige TWSG1 ELISA Kits) may be beneficial for AD prevention and treatment.
SNX15 (zeige SNX15 ELISA Kits) regulates the recycling of APP (zeige APP ELISA Kits) to cell surface and, thus, its processing for Abeta (zeige APP ELISA Kits) generation.
Immunohistochemical analysis confirmed increased amount of NOS1 (zeige NOS1 ELISA Kits) protein in neuronal somata and processes in the perilesional cortex in APP (zeige APP ELISA Kits)/PS1 (zeige PSEN1 ELISA Kits)-severe traumatic brain injury(TBI) mice compared to APP (zeige APP ELISA Kits)/PS1 (zeige PSEN1 ELISA Kits)-sham (p < 0.05) or Wt-sTBI mice (p < 0.01).
our findings indicate that sortilin (zeige SORT1 ELISA Kits) is a beneficial protein for the reduction of amyloid pathology in APP (zeige APP ELISA Kits)/PS1 (zeige PSEN1 ELISA Kits) mice by promoting APP (zeige APP ELISA Kits) degradation
a 99-aa C-terminal fragment of APP (zeige APP ELISA Kits),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 (zeige INPPL1 ELISA Kits) axis links Abeta (zeige APP ELISA Kits) neurotoxicity to tau pathology by dysregulating phosphoinositide metabolism, providing insight into therapeutic potential against Alzheimer's disease.
results suggest that PrP(C (zeige PRNP ELISA Kits)) recognizes structural features common to both Abeta (zeige APP ELISA Kits) oligomers and fibril ends and that this interaction could contribute to the neurotoxic effect of Abeta (zeige APP ELISA Kits) aggregates.
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.
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 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 A4 protein homolog
, amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease)
, amyloid A4
, amyloidogenic glycoprotein
, protease nexin II