A rescue factor abolishing neuronal cell death by a wide spectrum of familial Alzheimer's disease genes and Abeta -- Data Supplement - Supplemental Data -- Proceedings of the National Academy of Sciences

Supplementary material for Hashimoto et al. (2001) Proc. Natl. Acad. Sci. USA 98 (11), 6336–6341. (10.1073/pnas.101133498)

Supplemental Figure 7 Fig. 7.
Effect of synthetic Humanin (sHN) and its derivatives on neuronal cell viability decreased by familial Alzheimer’s disease (FAD) genes and expression of FAD genes. (A) Cell viability measurement by metabolic activity of viable cells. F11 cells were transfected with pcDNA (vec) or pcDNA encoding V642I-APP, M146L-PS-1, or N141I-PS-2 in the presence or absence of 10 µM sHN, 10 nM synthetic S14G HN (sHNG), or 10 µM synthetic C8A HN (sHNA) for 72 hr. Cell viability was measured by WST-8 assay; the y axis indicates the absorbance at 450 nm wave length (arbitrary units per well). (B) Lack of the effect of sHN, sHNG, or sHNA on the expression of V642I-APP, M146L-PS-1, or N141I-PS-2. F11 cells were transfected with V642I-APP (Top), M146L-PS-1 (Bottom), or N141I-PS-2 cDNA (Middle) and were treated with 10 µM sHN, sHNG, or sHNA. At 72 hr after the onset of transfection, cell lysates were submitted to immunoblot analysis with antibodies for the cognate FAD gene products. Arrows indicate corresponding FAD proteins in a holoprotein form.