Amyloid beta (Abeta) Kits ELISA

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 (264) et beta Amyloid Protéines (3) et beaucoup plus de produits pour cette protéine.

list all ELISA KIts Gène GeneID UniProt
Abeta 351 P05067
Anti-Rat Abeta Abeta 54226 P08592
Anti-Souris Abeta Abeta 11820 P12023
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Catalogue No. Reactivité Sensibilité Gamme Images Quantité Fournisseur Livraison Prix Détails
Humain 10 pg/mL 312-20000 pg/mL Representative Standard Curve 96 Tests Connectez-vous pour afficher 15 to 16 Days

Plus Kits ELISA pour beta Amyloid partenaires d'interaction

Human Amyloid beta (Abeta) interaction partners

  1. genetic manipulation of Sirt3 revealed that amyloid-beta increased levels of total tau acetylated tau through its modulation of Sirt3.

  2. brain. In the present study, two familial Ab42 mutations, namely A2V (harmful) and A2T (protective) have been analyzed and compared with the wild-type (WT) by performing all-atom molecular dynamics (MD) simulations in the absence and presence of curcumin, a well-known inhibitor of Abeta plaque formation. Mutant A2V was found to exhibit highest stability followed by WT and mutant A2T in the absence of curcumin

  3. 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.

  4. A physical interaction between nicastrin (hNCT) and the gamma-secretase substrate amyloid beta-protein precursor (APPC100) confirmed the functionality of hNCT as a substrate recognizer.

  5. ethanol-induced eIF2alpha phosphorylation stimulates COX-2 expression and PGE2 production which induces the BACE1 expression and Abeta production via EP-2 receptor-dependent PKA/CREB pathway.

  6. Western diet (WD) dramatically increases ABETA levels and generates pyroglutamate-ABETA deposits.

  7. This study demonstrated that the APP21 transgenic rats develop age-dependent cognitive impairment and accelerated white matter inflammation.

  8. Data suggest that kinetics of degradation/proteolysis versus of aggregation of amyloid beta(1-40) and amyloid beta(1-42) at specific concentrations of amyloid beta, cathepsin B, and cystatin C can be modeled and predicted.

  9. In vitro neuroprotective effects of naringenin nanoemulsion against beta-amyloid toxicity through the regulation of amyloidogenesis and tau phosphorylation.

  10. The results of study demonstrate that different degradation pathways play distinct roles in the removal of Abeta42 aggregates and in disease progression. These findings also suggest that pharmacologic treatments that are designed to stimulate cellular degradation pathways in patients with AD should be used with caution.

  11. This data demonstrates a specific function of APP or its metabolites is involved in the changes that occur during high fat diet-induced obesity.

  12. Our study provides new insights into the regulation of APP pre-mRNA processing, supports the role for nELAVLs as neuron-specific splicing regulators and reveals a novel function of AUF1 in alternative splicing.

  13. Data show that phospholipase D3 (PLD3) functions in endosomal protein sorting and plays an important role in regulating amyloid precursor protein (APP) processing.

  14. Data show that amyloid precursor protein (APP) dimerization affects its interaction with LDL receptor related protein 1 (LRP1) and LDL-receptor related protein SorLA (SorLA), suggesting that APP dimerization modulates its interplay with sorting molecules and in turn its localization and processing.

  15. overexpression of APP may promote the onset of seborrhoeic keratosis and is a marker of skin ageing and UV damage.

  16. Amyloid fibrils of Abeta1-40 peptide can effectively initiate amyloid formation in different globular proteins and metabolites, converting native structures into beta-sheet rich assemblies. Structural and biophysical properties of the resultant protein fibrils display amyloid like characteristic features.

  17. Structural and biochemical differences between the Notch and the amyloid precursor protein transmembrane domains.

  18. Gnetin C may thereby prevent Abeta toxicity by suppressing BACE1 and enhancing MMP-14, together with reducing both internalization and oligomerization of exogenous Abeta monomers.

  19. Amyloid precursor protein (APP) binds the HIV-1 Gag polyprotein, retains it in lipid rafts and blocks HIV-1 virion production and spread.

  20. ABETA(1-42) doses >5 microM inhibited the growth of U87 cells compared with the 0 microM group after 24 and 48 h treatment.

Mouse (Murine) Amyloid beta (Abeta) interaction partners

  1. 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.

  2. 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.

  3. Conformational changes in a mouse model of Alzheimer's disease-linked amyloid beta and APP take place before the amyloids plaques can be seen.

  4. These results support the proposition that Aβ release during thrombosis serves as part of a natural defense against infection.

  5. These data suggest a novel regulatory function of juxta- and intra-membrane domains on the metabolism and function of APP.

  6. Inflammasome-derived cytokine IL18 suppresses amyloid-induced seizures in Alzheimer-prone mice.

  7. pharmacological inhibition of PARP-1 reversed both particulate matter-induced Abeta increase and glial activation.

  8. 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.

  9. 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.

  10. This study demonstrated that APP as a novel receptor for Slit ligand mediating axon guidance and neural circuit formation.

  11. 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.

  12. 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.

  13. ADAP KO mice developed glomerular pathology. ADAP KO podocytes lack cell protrusions with actin cytoskeleton forming circumferential stress fibers.

  14. Therefore, APP modulates Nav1.6 sodium channels through a Go-coupled JNK pathway, which is dependent on phosphorylation of APP at Thr668.

  15. These findings suggest that in the absence of CLU, Abeta clearance shifts to perivascular drainage pathways, resulting in fewer parenchymal plaques but more CAA because of loss of CLU chaperone activity, complicating the potential therapeutic targeting of CLU for AD.

  16. Chronic Dyrk1 inhibition reversed cognitive deficits in Alzheimer's disease transgenic mice via reduction of APP and phosphorylated tau pathology.

  17. The findings provide a model for initiation of synaptic dysfunction whereby exposure to physiologic levels of amyloid beta for a prolonged period of time causes microstructural changes at the synapse which result in increased transmitter release, failure of synaptic plasticity, and memory loss.

  18. The results of the present study substantiate that cGMP has a role in the endocytic pathway of APP and suggest a scenario where the cyclic nucleotide enhances the production of Abeta by favoring the trafficking of APP from the cell cortex to the endolysosomal compartment.

  19. Study showed that the APP Osaka mutation has dual effects: it causes a loss-of-function of APP and gain-of-toxic-function of Abeta, though the latter seems to come out only after the former causes GABAergic depletion. Also present OSK-KI mice as a mouse model to replicate the hereditary form of recessive familial Alzheimer's disease.

  20. Enhancing mitochondrial proteostasis reduces amyloid-beta proteotoxicity

beta Amyloid (Abeta) profil antigène

Antigen Summary

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.

Gene names and symbols associated with Amyloid beta (Abeta) Kits ELISA

  • amyloid beta precursor protein (APP) anticorps
  • amyloid beta precursor protein (app) anticorps
  • amyloid beta precursor protein (App) anticorps
  • amyloid beta (A4) precursor protein (App) anticorps
  • aaa anticorps
  • Abeta anticorps
  • Abpp anticorps
  • ad1 anticorps
  • Adap anticorps
  • Ag anticorps
  • appi anticorps
  • betaApp anticorps
  • ctfgamma anticorps
  • Cvap anticorps
  • E030013M08Rik anticorps
  • PN-II anticorps
  • pn2 anticorps

Protein level used designations for Amyloid beta (Abeta) Kits ELISA

alzheimer disease amyloid protein , amyloid beta A4 protein , beta-amyloid peptide , cerebral vascular amyloid peptide , peptidase nexin-II , preA4 , 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) , ABPP , AG , amyloid A4 , amyloidogenic glycoprotein , appican , protease nexin II

351 Homo sapiens
448208 Xenopus (Silurana) tropicalis
100427716 Macaca mulatta
54226 Rattus norvegicus
11820 Mus musculus
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