Amyloid Beta Mouse Monoclonal Antibody | FR | MédiMabs

Amyloid Beta Mouse Monoclonal Antibody

Amyloid Beta Mouse Monoclonal Antibody

Amyloid Beta Mouse Monoclonal Antibody

MM-0015 -- anti-Amyloid Beta
$355,00/100 µl
Pour les prix de gros, nous contacter.
NUMÉRO : MM-0015
  • Nom du produit
    Amyloid Beta Mouse Monoclonal Antibody
  • Serveur
  • Clonality
  • Tested Applications
    Immunohistochemistry (IHC), Electron microscopy immunocytochemistry (ICC), Immunoprecipitation (IP)
  • Research Area(s)
  • Immunogen
    Full lenght Amyloid beta
  • Modifications
  • Clone ID
  • DataSHEET
  • Isotype
  • Conjugation
  • Reactivity
    Both neuritic and diffuse plaques can be detected as well as cerebrovascular amyloid in affected cortex of Alzheimer’s disease (AD) brain by ICC
  • Specificity
    Human and Mouse
  • Purification
    Non Purified
  • Target Name
    Amyloid Beta
  • Storage Buffer
    Protein free tissue culture supernatant
  • Alias
    Beta-amyloid ABP amyloid peptide
  • Format
    100 µl
  • Background
    Progressive deposition of insoluble aggregates of the 39 to 43 amino acid amyloid β (Aβ) peptide derived from the proteolytic cleavage of the amyloid β-protein precursor (AβPP), gives rise to one of the pathological hallmarks of Alzheimer’s disease (AD). The formation of Aβ fragments is a critical determinant in unleashing AD neuropathology.

For laboratory research only, not for drug, diagnostic or other use.

  • Reelin-immunoreactive neurons in entorhinal cortex layer II selectively express intracellular amyloid in early Alzheimer's disease
  • Intraneuronal Amyloid Beta Accumulation Disrupts Hippocampal CRTC1Dependent Gene Expression and Cognitive Function in a Rat Model of Alzheimer Disease
  • Stereological estimation of neuron number and plaque load in the hippocampal region of a transgenic rat model of Alzheimer’s disease
  • The Multi-Target Drug M30 Shows Pro-Cognitive and Anti-Inflammatory Effects in a Rat Model of Alzheimer’s Disease
  • Longitudinal testing of hippocampal plasticity reveals the onset and maintenance of endogenous human Aß-induced synaptic dysfunction in individual freely behaving pre-plaque transgenic rats: rapid reversal by anti-Aß agents
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