Amyloid beta Proteine (Abeta)

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 (178) und beta Amyloid Kits (1) und viele weitere Produktgruppen zu diesem Protein an.

alle Proteine anzeigen Gen GeneID UniProt
Abeta 351 P05067
Ratte Abeta Abeta 54226 P08592
Maus Abeta Abeta 11820 P12023
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Katalog Nr. Origin Quelle Konjugat Bilder Menge Lieferzeit Preis Details
Escherichia coli (E. coli) Human Unkonjugiert 50 μg 9 bis 11 Tage
Escherichia coli (E. coli) Human Unkonjugiert   100 μg 11 bis 16 Tage
Synthetic Human Unkonjugiert   1 mg 3 bis 4 Tage

Abeta Proteine nach Spezies und Herkunft

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Weitere Proteine zu Amyloid beta (Abeta) Interaktionspartnern

Human Amyloid beta (Abeta) Interaktionspartner

  1. Thirteen of 148 (8.8%) individuals had possible pathogenic APP, PSEN1, or PSEN2 variants, including 2 (15.4%) APP variants, 8 (61.5%) PSEN1 variants, and 3 (23.1%) PSEN2 variants

  2. Synaptic dysfunction caused by presenilin-1 mutant and amyloid precusor protein duplication secretomes is mediated by Abeta peptides, whereas trisomy of chromosome 21 (trisomy 21) neuronal secretomes induce dysfunction through extracellular tau.

  3. In invasive cells, MT1-MMP endocytosis to the endolysosomal reservoir compartment requires flotillin 1 and flotillin 2.

  4. These data demonstrate a key role for proteolysis of the C-terminal of APP by gamma-secretase in neuronal dysfunction in monogenic Alzheimer's disease.

  5. a Drosophila Alzheimer's disease (AD) model expressing a secreted form of human amyloid-beta42 peptide showed that it recapitulates key aspects of AD pathology, including neuronal death and impaired long-term memory.

  6. Beta-amyloid peptide(1-42) (Abeta1-42) : phosphorylated Tau (p-Tau) ratio has potential for being implemented in the clinical routine for differential diagnosis between AD and other dementias and to distinguish underling pathology such as neurodegenerative disease.

  7. CIP2A-mediated PP2A inhibition drives tau/APP hyperphosphorylation and increases APP beta-cleavage and Abeta production.

  8. miR-346 plays a role in upregulation of APP in the CNS and participates in maintaining APP regulation of Fe, which is disrupted in late stages of AD.

  9. analysis of the interaction between monomeric Abeta40/42 and HSA using surface plasmon resonance spectroscopy

  10. Structural dynamics of dipeptides and ABETA (25-35) in aqueous solution were demonstrated

  11. We found that individuals with elevated beta-amyloid aggregation had a blunted cerebrovascular response compared to non-elevated individuals

  12. in cholinergic neurons from Drosophila, beta-amyloid (Abeta) peptides Abeta40 and Abeta42 both induce an increase in spontaneous activity.

  13. These data indicate that the sAbeta1-42 may play a dual role during inflammatory process, wherein, it may be involved in protecting the cells from inflammatory damage due to TNF-alpha.

  14. We observed that over-expression of PIEZO1 in HEK293 cells increased cell migration velocity ~10-fold, and both enantiomeric A-beta peptides and GsMTx4 independently inhibited migration, demonstrating involvement of PIEZO1 in cell motility.

  15. We found amyloid measures to be sensitive early on in predicting subsequent early tau deposition

  16. APP facilitate an early step in thrombus formation when amyloid beta (Abeta) peptides accumulate in cerebral vessel walls or atherosclerotic plaques.

  17. The differing patterns in cerebral amyloid angiopathy within individuals may relate to the relative tissue burdens of the two major forms of Abeta, with higher levels of Abeta40 promoting a more 'aggressive' form of CAA, and higher levels of Abeta42(3) favouring a greater plaque burden

  18. we provide a novel method to convert standardized uptake value ratios-levels into PET-Abeta phase estimates that can be easily translated into neuropathological phases of Abeta-deposition

  19. Influence of the familial Alzheimer's disease-associated T43I mutation on the transmembrane structure and gamma-secretase processing of the C99 peptide

  20. results may explain the role of hAChE-S in Abeta deposition and aggregation, as amyloidogenic hAChE-S beta-sheet species might seed Abeta aggregation.

Mouse (Murine) Amyloid beta (Abeta) Interaktionspartner

  1. show a novel function for Par3 in regulating polarized convergence between APP and BACE1 in hippocampal neurons

  2. Proteasome inhibition precludes APP axonal transport by enhancing its endo-lysosomal delivery, where beta-cleavage is induced.

  3. CIP2A-mediated PP2A inhibition drives tau/APP hyperphosphorylation and increases APP beta-cleavage and Abeta production.

  4. App(-/-) mice have higher levels of insulin-degrading enzyme (IDE) mRNA, protein, and activity. Regulation of IDE by APP was widespread across numerous tissues, including liver, skeletal muscle, and brain as well as cell types within neural tissue. App-/- mice failed to develop impairment of glucose tolerance on a high-fat, high-sucrose diet.

  5. The findings demonstrate that chronic noise exposure exacerbated Alzheimer's disease-like neuropathology, possibly by disrupting Wnt signaling and triggering aberrant tau hyperphosphorylation and amyloid beta peptides in the prefrontal cortex and hippocampus.

  6. A novel lysosome-to-mitochondria signaling pathway disrupted by amyloid-beta oligomers.

  7. Together these data indicate that ONA induces APP expression and that gamma-secretase cleavage of APP releases AICD, which upregulates JNK3 leading to RGC death. This pathway may be a novel target for neuronal protection in optic neuropathies and other forms of neurotrauma.

  8. In addition to regulating aspects of neuronal metabolism, APP is an important regulator of whole body energy expenditure and glucose homeostasis under high fat feeding conditions.

  9. 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 .

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

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

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

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

  14. 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.

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

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

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

  18. 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.

  19. 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.

  20. 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.

beta Amyloid (Abeta) Protein Überblick

Protein Überblick

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.

Genbezeichner und Symbole assoziert mit Amyloid beta Proteine (Abeta)

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

Bezeichner auf Proteinebene für Amyloid beta Proteine (Abeta)

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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