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 (258) 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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Top beta Amyloid Kits ELISA sur anticorps-enligne.fr

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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
$550.00
Détails

Plus Kits ELISA pour beta Amyloid partenaires d'interaction

Human Amyloid beta (Abeta) interaction partners

  1. The neuronal specific alpha3 (alpha3)-subunit of the plasma membrane enzyme Na, K-ATPase (NKA) is a new binding partner of sAPPalpha.

  2. Aggregation processes of ABETA on living cells and cytotoxic events were monitored by fluorescence techniques. ABETA formed amyloids after forming oligomers composed of approximately 10 ABETA molecules. The formation of amyloids was necessary to activate apoptotic caspase-3 and reduce the ability of the cell to proliferate; this indicated that amyloid formation is a key event in ABETA-induced cytotoxicity.

  3. esults suggest that P-gp plays important role in mediating rivastigmine non-cholinergic beneficial effects, including Abeta brain load reduction, neuroprotective and anti-inflammatory effects in the AD mouse models.

  4. Immature intracellular aggregates are more toxic than mature fibrillar ABETA(1-42).

  5. Downregulation of C9orf72 in non-neuronal human cells overexpressing amyloid-beta protein precursor (AbetaPP) resulted in increased levels of secreted AbetaPP fragments and Abeta, while levels of AbetaPP or its C-terminal fragments (CTFs) remained unchanged. In neuronal cells, AbetaPP and C83 CTF levels were decreased upon C9orf72 knockdown, but those of secreted AbetaPP fragments or Abeta remained unchanged.

  6. N-terminal mutations can affect Abeta fibril and oligomer formation, despite lying outside the core amyloid region of Abeta. Of the three factors that may influence Abeta-mediated toxicity (primary structure of Abeta, assembly structure and cellular responses), results suggest that it is more the assembly structure that correlates with effects on cell viability.

  7. The Swedish variant was a more potent co-activator of Wnt-PCP signalling than wild-type APP and, unlike wild-type APP, which co-activates Wnt beta-catenin signalling, APPSwe suppressed this branch of Wnt.

  8. Among hip fracture patients, 88.6% of the cognitively normal (Clinical Dementia Rating-CDR 0; n = 70) and 98.8% with mild cognitive impairment (CDR 0.5; n = 81) fell in the abnormal biomarker categories by CSF Abeta42/40 ratio, p-tau, and t-tau measures.

  9. FNDC5 significantly affects beta-cleavage of APP via the interaction with APP.

  10. uncovered for the first time a phenomenon of chaperone antagonism on BACE1-mediated Abeta42 generation.

  11. This study investigated the assembly mechanisms of dimeric ABETA 16-22 and found that the fibril formation rate is predominantly controlled by the total beta-strand content.

  12. Data suggest that the substitution of alanine by valine at position 2 of the amyloidogenic peptide affect the lateral interactions between fibrils, promoting a more compact, aligned and uniform structure which explains its aggressiveness in homozygous carriers and its prophylactic effect in heterozygous carriers.

  13. Solution NMR allowed us to define the secondary structure of this Abeta dimer, which shows interlocking contacts between C-terminal peptide strands. Thus, we present a novel Abeta oligomer that resists conversion to fibrils and remains stable for more than one year.

  14. Data suggest that antiinflammatory agents, non steroidal (NSAIDs) bind to amyloid beta (Abeta) protein leading to the blockage of hydrophobic site which might prevent incoming Abeta molecules from extending the fibril.

  15. Findings suggest that the polymorphisms of amyloid-beta (Abeta) fibril structures are caused by differences in the surrounding ionic environment.

  16. Young healthy adults carrying APOE epsilon4 and APP/presenilin-1/2 displayed different hippocampus functional connectivity patterns

  17. X-box binding protein 1 overexpression at an early stage reversed Abeta-induced early death without affecting learning performance in the Abeta42 transgenic flies. PERK activation was determined to only enhance Abeta-induced learning deficits.

  18. data suggests that the hydrophobic interactions between beta-casein and Abeta1-42 play an important role in the burial of the hydrophobic part of the Abeta1-42.

  19. APP-Knockout astrocytes have reduced cholesterol and elevated levels of sterol regulatory element-binding protein (SREBP) target gene transcripts and proteins, which were both downstream consequences of reduced lipoprotein endocytosis.

  20. Identified TMEM30A as a candidate partner for beta-carboxyl-terminal fragment (betaCTF) of amyloid-beta precursor protein (APP). TMEM30A physically interacts with betaCTF in endosomes and may impair vesicular traffic, leading to abnormally enlarged endosomes. Data suggested that TMEM30A is involved in betaCTF-dependent endosome abnormalities that are related to Abeta overproduction

Mouse (Murine) Amyloid beta (Abeta) interaction partners

  1. 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.

  2. 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.

  3. 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.

  4. 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.

  5. 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.

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

  7. 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.

  8. 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.

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

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

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

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

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

  14. 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.

  15. 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.

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

  17. 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.

  18. 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.

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

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

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

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