Recombinant Human Amyloid Precursor Protein Fc Chimera, CF Summary
|Human Amyloid-beta A4 (Isoform APP695)|
Accession # P05067-4
CF stands for Carrier Free (CF). We typically add Bovine Serum Albumin (BSA) as a carrier protein to our recombinant proteins. Adding a carrier protein enhances protein stability, increases shelf-life, and allows the recombinant protein to be stored at a more dilute concentration. The carrier free version does not contain BSA.
In general, we advise purchasing the recombinant protein with BSA for use in cell or tissue culture, or as an ELISA standard. In contrast, the carrier free protein is recommended for applications, in which the presence of BSA could interfere.
|Formulation||Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose.|
|Reconstitution||Reconstitute at 500 μg/mL in PBS.|
|Shipping||The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.|
|Stability & Storage:||
Amyloid precursor protein (APP) is a type I membrane protein with several isoforms due to alternative splicing. Of the three major splice isoforms of APP (APP695, APP751, and APP770) APP695 is the predominant neuronal form from which Amyloid beta peptide and transcriptionally-active cleaved intracellular domain of APP (AICD) are preferentially generated by selective processing through the amyloidogenic pathway (1). Human APP695 consists of a 17 amino acid (aa) signal sequence, a 607 aa extracellular domain (ECD), a 24 aa transmembrane domain, and a 47 aa cytoplasmic domain. Within the ECD, human APP695 shares 97% aa sequence identity with mouse and rat APP695. Amyloid beta is a major molecule implicated in pathogenesis of Alzheimer's disease (AD) and related dementias (2). AICD regulates expression by direct promoter binding of multiple genes, including APP itself, the beta-secretase, BACE-1 and the Amyloid beta-degrading enzyme, Neprilysin (3, 1). As such, APP695 plays an important role in brain development, learning and memory, synaptic plasticity, and neurodegeneration including AD (4).
- Nalivaeva, N.N. and Turner A. J. (2013) FEBS Lett. 587:2046.
- Haass, C. (2004) EMBO J. 23:483.
- Passer, B. et al. (2000) J. Alzheimers Dis. 2:289.
- Benilova, I. et al. (2012) Nat. Neurosci. 15:349.
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