Introduction from Drug peptide supply about:beta-Amyloid (1-42) human
|English name||beta-Amyloid (1-42) human|
|Package||1mg;5mg;10mg;50mg;100mg,1g or according to customer’s detail requirement.|
|Product English synonyms||AmyloidβREFDUPL:Beta-Amyloid(1-42),sodiumsalt;Β-AMYLOIDPEPTIDE(1-42),RAT|
Introduction of β-Amyloid (1-42)(human)
This peptide is well suited to the quantitative determination of A 42 peptide. Alzheimer’s disease (AD) is characterized by the presence of extracellular plaques and intracellular neurofibrillary tangles (NFTs) in the brain. The major protein component of these plaques is beta amyloid peptide (A), a 40- to 43- amino-acid peptide cleaved from amyloid precursor protein by secretase (BACE) and a putative (gamma) secretase. Increased release of the ‘longer forms’ of A peptide, A 42 and A 43, which have a greater tendency to aggregate than A 40, occurs in individuals expressing certain genetic mutations, expressing certain ApoE alleles or may other, still undiscovered factors.
Mechanism of β-amyloid peptide Aβ1-42 peptide
Numerous mutations identified in the gene encoding beta-amyloid precursor protein (βAPP) are associated with early-onset familial Alzheimer’s disease. Studies have also shown that mutations in the genes encoding presenilin 1 and presenilin 2 alter the processing of βAPP, resulting in increased extracellular concentrations of the amyloid β peptide Aβ1-42 (43) relative to Aβ1-40. Biophysical and biochemical experiments have shown that Aβ1-42(43) can act as a catalyst for the aggregation and deposition of β-amyloid peptide (Aβ), which has neurotoxic effects associated with senile plaque formation. Additionally, antibodies recognizing Aβ1-42 showed increased long-form peptides in presenilin and βAPP mutants, while other studies used Aβ-specific antibodies to prevent Aβ fibrillar aggregation in vitro. Amino acid sequence verified by amino acid analysis or sequencing. This product is supplied in a non-neurotoxic form prior to the pre-incubation step. The emergence of toxicity has recently been shown to correlate with the degree of beta-sheet structure. For neurotoxicity studies and substrate cleavage assays.
How to buy beta-Amyloid (1-42) human in the U. S.
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