Amyloid Precursor Protein A Practical Approach by Weiming Xia, Huaxi Xu

By Weiming Xia, Huaxi Xu

Within the look for a good therapy for Alzheimer's ailment, APP is a special version protein that illustrates the big range of simple and complex characterization concepts on hand. Exploring various organic innovations to explain the constitution and serve as of this transmembrane protein, this article provides every one process with targeted, step by step protocols to accomplish reproducible effects and supply a framework for learning different membrane proteins.

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In vivo memapsin 2 may be regulated by factors including expression, post-translational modifications and membrane component compositions such as “lipid rafts” and endocytotic and vesicular trafficking to acidic compartments such as endosomes. Nonetheless, small peptide substrates representing the β-secretase cleavage site in APP are capably cleaved by memapsin 2,5,12 demonstrating the independence of in vivo biochemical regulation from its fundamental proteolytic function. Similarly, retroviral proteases demonstrate complex in vivo characteristics, requiring dimerization in the form of gag-pol precursor proteins with subsequent activation from these precursor multiproteins.

Fit of the linear portion of the signal to a linear model produces a typical signal of 10-3 fluorescence units per second (FU/sec). 1. 15 However, this correction is not necessary in the determination of the inhibition constant Kiapp (see below) because relative initial velocities are determined at a fixed substrate concentration. 3 SYNTHESIS OF MEMAPSIN 2 INHIBITORS BASED ON APP SEQUENCE Transition state theory indicates that an enzyme will bind most tightly to its substrate when the substrate adopts a conformation approximating the transition state in the progression toward product formation.

Structure 6, 637, 1998. 31. U. et al. From differentiation to proliferation: the secretory amyloid precursor protein as a local mediator of growth in thyroid epithelial cells. Proc. Natl. Acad. Sci. USA 95, 1770, 1998. 32. A. C. Amyloid precursor protein modulates the interaction of nerve growth factor with p75 receptor and potentiates its activation of trkA phosphorylation. Mol. Brain. Res. 56, 125, 1998. 33. Henry A. et al. Inhibition of platelet activation by the Alzheimer’s disease amyloid precursor protein.

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