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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. De plus, nous expédions beta Amyloid Anticorps (277) et et beaucoup plus de produits pour cette protéine.
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The authors show that APP (Montrer APP Kits ELISA) can physically interact with KCC2 (Montrer SLC12A5 Kits ELISA), a neuron-specific K(+)-Cl(-) cotransporter (Montrer SLC12A4 Kits ELISA) that is essential for Cl(-) homeostasis and fast GABAergic inhibition.
beta-amyloid interacts with fibrinogen and factor XII (Montrer F12 Kits ELISA). These interactions can lead to increased clotting, abnormal clot (Montrer TXNDC17 Kits ELISA) formation, persistent fibrin deposition, and generation of proinflammatory molecules.
Abeta (Montrer APP Kits ELISA) activates FXII (Montrer F12 Kits ELISA), resulting in FXI (Montrer F11 Kits ELISA) activation and thrombin (Montrer F2 Kits ELISA) generation in human plasma, thereby establishing Abeta (Montrer APP Kits ELISA) as a possible driver of prothrombotic states
Data suggest that aggregates of amyloid beta(1-40) induce excessive generation of reactive oxygen species, MAPK (Montrer MAPK1 Kits ELISA)/NFkappaB (Montrer NFKB1 Kits ELISA) signaling activation, and NLRP3 (Montrer NLRP3 Kits ELISA) inflammasome activation in retinal pigment epithelial cells mimicking changes seen in age-related macular degeneration; this mechanism is dependent on NADPH oxidase (Montrer NOX1 Kits ELISA).
These results demonstrate a stage-dependent plasma Abeta (Montrer APP Kits ELISA) increase that is augmented by loss of glomerulotubular integrity, low body weight, and inflammation, demonstrating a multifaceted role of renal dysfunction in Abeta (Montrer APP Kits ELISA) retention.
Combining a murine APP (Montrer APP Kits ELISA)-deficient and a human APP (Montrer APP Kits ELISA)-transgenic strain, we were able to analyse the progression of the cortical amyloidosis independent of the murine variant. The lack of endogenous mAPP (Montrer XPNPEP2 Kits ELISA) 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 (Montrer APP Kits ELISA) to disrupt synaptic activity.
activation of mTOR (Montrer FRAP1 Kits ELISA) signalling via RHEB (Montrer RHEB Kits ELISA) over-expression inhibited the starvation-induced autophagy but did not affect trafficking of tf-Amyloid precursor protein (APP (Montrer APP Kits ELISA)). These results show tf-APP (Montrer APP Kits ELISA) can be used to determine how APP (Montrer APP Kits ELISA) is trafficked through the lysosomal system of the cell.
Study found that FERMT2 (Montrer FERMT2 Kits ELISA) (a beta3-integrin (Montrer ITGB3 Kits ELISA) co-activator) was significantly associated with a variation in cerebrospinal fluid Abeta (Montrer APP Kits ELISA) peptide levels in 2886 Alzheimer's disease cases.Under-expression of FERMT2 (Montrer FERMT2 Kits ELISA) increases Abeta (Montrer APP Kits ELISA) peptide production by raising levels of mature APP (Montrer APP Kits ELISA) at the cell surface and facilitating its recycling
This study demonstrates the neuroprotective effect of TSG (Montrer TWSG1 Kits ELISA) on APP (Montrer APP Kits ELISA) expression, suggesting that TSG (Montrer TWSG1 Kits ELISA) may be beneficial for AD prevention and treatment.
SNX15 (Montrer SNX15 Kits ELISA) regulates the recycling of APP (Montrer APP Kits ELISA) to cell surface and, thus, its processing for Abeta (Montrer APP Kits ELISA) generation.
Immunohistochemical analysis confirmed increased amount of NOS1 (Montrer NOS1 Kits ELISA) protein in neuronal somata and processes in the perilesional cortex in APP (Montrer APP Kits ELISA)/PS1 (Montrer PSEN1 Kits ELISA)-severe traumatic brain injury(TBI) mice compared to APP (Montrer APP Kits ELISA)/PS1 (Montrer PSEN1 Kits ELISA)-sham (p < 0.05) or Wt-sTBI mice (p < 0.01).
our findings indicate that sortilin (Montrer SORT1 Kits ELISA) is a beneficial protein for the reduction of amyloid pathology in APP (Montrer APP Kits ELISA)/PS1 (Montrer PSEN1 Kits ELISA) mice by promoting APP (Montrer APP Kits ELISA) degradation
a 99-aa C-terminal fragment of APP (Montrer APP Kits ELISA),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 (Montrer INPPL1 Kits ELISA) axis links Abeta (Montrer APP Kits ELISA) neurotoxicity to tau pathology by dysregulating phosphoinositide metabolism, providing insight into therapeutic potential against Alzheimer's disease.
results suggest that PrP(C (Montrer PRNP Kits ELISA)) recognizes structural features common to both Abeta (Montrer APP Kits ELISA) oligomers and fibril ends and that this interaction could contribute to the neurotoxic effect of Abeta (Montrer APP Kits ELISA) 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