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Additional resources for Cellular Mechanisms of Alzheimer's Disease: Neurodegenerative Diseases 2006
228 Neurodegenerative Dis 2006;3:227–232 Taken together, these results suggest that presenilins function in the embryonic development of most, if not all, animals and facilitate Notch signaling. Although redundant in their enzymatic activity, sel-12 and hop-1 mutants differ in the phenotype that is the consequence of their deletion. Whereas hop-1 null mutants are superficially inconspicuous, all known mutations in sel-12 have a strong egg-laying defect, and also display additional deficits not obviously linked to egg-laying.
35 Mandelkow EM, Mandelkow E: Tau in Alzheimer’s disease. Trends Cell Biol 1998; 8: 425–427. 36 von Bergen M, Li L, Mandelkow E: Intrinsic fluorescent detection of tau conformation and aggregation. Methods Mol Biol 2005; 299:175–184. 37 Biernat J, Gustke N, Drewes G, Mandelkow EM, Mandelkow E: Phosphorylation of Ser262 strongly reduces binding of tau to microtubules: distinction between PHF-like immunoreactivity and microtubule binding. Neuron 1993;11:153–163. 38 Seubert P, Mawaldewan M, Barbour R, Jakes R, Goedert M, Johnson GVW, Litersky J, Schenk D, Lieberburg I, Trojanowski J, Lee VMY: Detection of phosphorylated Ser(262) in fetal tau, adult tau, and paired helical filament tau.
57 Chen XH, Siman R, Iwata A, Meaney DF, Trojanowski JQ, Smith DH: Long-term accumulation of amyloid-beta, beta-secretase, presenilin-1, and caspase-3 in damaged axons following brain trauma. Am J Pathol 2004;165:357–371. 58 Heber S, Herms J, Gajic V, Hainfellner J, Aguzzi A, Rulicke T, von Kretzschmar H, von Koch C, Sisodia S, Tremml P, Lipp HP, Wolfer DP, Muller U: Mice with combined gene knock-outs reveal essential and partially redundant functions of amyloid precursor protein family members.
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