Amyloid beta (Abeta) ELISA Kits

Abeta encodes a cell surface receptor and transmembrane precursor protein that is cleaved by secretases to form a number of peptides. Additionally we are shipping beta Amyloid Antibodies (181) and beta Amyloid Proteins (3) and many more products for this protein.

list all ELISA KIts Gene Name GeneID UniProt
Abeta 351 P05067
Anti-Rat Abeta Abeta 54226 P08592
Anti-Mouse Abeta Abeta 11820 P12023
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Catalog No. Reactivity Sensitivity Range Images Quantity Delivery Price Details
Human 10 pg/mL 312-20000 pg/mL Representative Standard Curve 96 Tests 15 to 16 Days

More ELISA Kits for beta Amyloid Interaction Partners

Human Amyloid beta (Abeta) interaction partners

  1. This study data demonstrate that low expression of APP is sufficient to drive histopathological and cognitive changes in mice without overexpression or excessive plaque deposition.

  2. This article reviews the current applications of Mass Spectrometry (MS) in the search for possible ABETA biomarkers of Alzheimer's disease to help the diagnosis of the disease. Recent examples of the important contributions that MS has given to prove or build theories on the molecular pathways involved with such terrible disease are also reviewed. [review]

  3. These findings indicate that under physiological conditions, expression of APP in cerebral vascular endothelium plays an important protective function by maintaining constitutive expression of eNOS .

  4. Abeta oligomers bind herpesvirus surface glycoproteins, accelerating beta-amyloid deposition and leading to protective viral entrapment activity in 5XFAD mouse and 3D human neural cell culture infection models against neurotropic herpes simplex virus 1 (HSV1) and human herpesvirus 6A and B.

  5. the inhibition of APPswe-induced secretion of inflammatory cytokines and the suppression of NF-kappaB activation by miR-15b were validated...Our study suggests that miR-15b inhibits Abeta accumulation through targetting NF-kappaB signaling and BACE1 and serves as a potential molecular target for Alzheimer's disease (AD) therapy

  6. This case study reports the first detailed clinical description of Val717Phe mutation, demonstrating amnestic AD phenotype with seizures, myoclonus, and Parkinsonism, and yields an overview of related autosomal dominantly inherited exonic mutations in the APP gene.

  7. CSF Abeta levels and white matter lesion loads (WM-LL) suggests a direct link between amyloid pathology and WM macrostructural and microstructural damage in Alzheimer's disease. There was increased WM-LL in Abeta(+) compared with both, healthy controls and Abeta(-) Alzheimer's patients.

  8. The findings reveal a novel mechanism whereby GSK3beta stimulates amyloidogenic processing of APP by phosphorylation of FE65 at threonine 579.

  9. A Toxic Conformer of Abeta42 with a Turn at 22-23 is a Novel Therapeutic Target for Alzheimer's Disease.

  10. Alzheimer's disease-associated TREM2 variants bind Abeta with equivalent affinity but show loss of function in terms of signaling and Abeta internalization.

  11. PKCdelta knockdown reduces BACE1 expression, BACE1-mediated APP processing, and Abeta production.

  12. recombination of APP in human neurons, occurring mosaically as thousands of variant 'genomic cDNAs' (gencDNAs); gencDNAs lacked introns and ranged from full-length cDNA copies of expressed, brain-specific RNA splice variants to myriad smaller forms that contained intra-exonic junctions, insertions, deletions, and/or single nucleotide variations

  13. results confirm the presence of Abeta seeds in archived c-hGH vials and are consistent with the hypothesized iatrogenic human transmission of Abeta pathology; this experimental confirmation has implications for both the prevention and the treatment of Alzheimer's disease, and prompt a review of the risk of iatrogenic transmission of Abeta seeds by medical and surgical procedures long recognized to pose a risk of prion ...

  14. Fpn and Heph co-localize, and FRET analysis indicated that the two proteins form an iron-efflux complex; in contrast, none of the full-length, cellular APP proteins exhibited Fpn co-localization or FRET

  15. we show that F-actin depolymerization in spines leads to a breakdown of the nano-organization of outwardly radiating F-actin rods in cortical neurons from APPswe/PS1DeltaE9 mice

  16. It was evident that on average only a single histidine residue coordinates Cu(II) in monomeric ABETA(1-42) at pH 6.1, in addition to 3 other oxygen or nitrogen ligands. Cu(II) coordination in ABETA(1-42) at pH 7.4 is similarly 4-coordinate with oxygen and nitrogen ligands, although an average of 2 histidine residues appear to coordinate at this pH.

  17. High carboxypeptidase A4 (CPA4) expression in triplenegative breast cancer (TNBC) cases is associated with low expression of E-cadherin and with the expression of cancer stem cell markers. Patients with TNBC and high levels of CPA4 expression have poorer prognosis compared with those with low CPA4 expression. Viability and migration are reduced, but E-cadherin expression is upregulated in CPA4-suppressed TNBC cells.

  18. Overexpression of AbetaPP in Muller cells (MC) induced strong antioxidant and anti-ER stress (PERK downregulation and GADD34 upregulation) responses accompanied by activation of the prosurvival branch of the unfolded protein response. It was also associated with upregulation of major genes involved in MC-controlled retinal homeostasis (KCNJ10, GS, and RLBP1) and protection against HNE-induced apoptosis.

  19. plasma amyloid beta protein level may predicti cognitive decline in patients suffering from chronic kidney disease.

  20. BIN1 rs744373 SNP is associated with increased tau but not beta-amyloid pathology, suggesting that alterations in BIN1 may contribute to memory deficits via increased tau pathology

Mouse (Murine) Amyloid beta (Abeta) interaction partners

  1. These findings indicate that under physiological conditions, expression of APP in cerebral vascular endothelium plays an important protective function by maintaining constitutive expression of eNOS .

  2. NRBF2 plays an important role in regulating degradation of APP-C-terminal fragments through modulating autophagy.

  3. These results provide evidence that both central circadian rhythms and local clock function influence Abeta dynamics and plaque formation.

  4. These data identified APP and APLP2 as modulators of normal myelination and demyelination/remyelination conditions.

  5. these findings suggest that endogenous Abeta is involved in memory forgetting in the normal brain.

  6. pterostilbene attenuated the neuroinflammatory response induced by Abeta1-42 in microglia through inhibiting the NLRP3/caspase-1 inflammasome pathway, indicating that pterostilbene might be an effective therapy for AD.

  7. Abeta40 and Abeta42 demonstrated distinct distribution kinetics in plasma and brain compartments, and insulin differentially modulated their distribution.

  8. APP/GBR complex formation links presynaptic GBR trafficking to Abeta formation.

  9. APP knockout increases synaptic GluA1, PSD-95 and synaptophysin expression and reduces drebrin expression.

  10. data indicate that Drp1 is a direct target of Cdk5, and Cdk5-mediated phosphorylation of Drp1 at Serine 579 regulates Abeta1-42 induced mitochondrial fission and neuronal toxicity.

  11. miR98 reduced the production of Abeta and improved oxidative stress and mitochondrial dysfunction through activation of the Notch signaling pathway by binding to HEY2 in Alzheimer's disease mice.

  12. Heme and Hb suppress immune activity of primary mouse astrocytes by reducing expression of several proinflammatory cytokines (e.g. RANTES (regulated on activation normal T cell expressed and secreted)) and the scavenger receptor CD36 and reducing internalization of Abeta(1-42) by astrocytes.

  13. extracellular cholesterol concentration in serum under conditions of Npc1 deficiency can influence intracellular cholesterol content/distribution and lysosomal efficacy, triggering the accumulation of toxic APP-cleaved products, eventually leading to cell death.

  14. Hippocampal mutant APP and amyloid beta-induced cognitive decline, dendritic spine loss, defective autophagy, mitophagy and mitochondrial abnormalities in a mouse model of Alzheimer's disease.

  15. This study provides a novel mechanism underlying aggregation of Abeta peptides via BC1 induction of APP mRNA translation.

  16. 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.

  17. 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.

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

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

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

beta Amyloid (Abeta) Antigen Profile

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) ELISA Kits

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

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

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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