The high-throughput techniques underlying a systems level analysis of biological organisms have emerged as powerful tools in the study of disease mechanisms. On the other hand, they require substantial funding and multidisciplinary skills. Therefore, basic biochemical/cell biology methods from molecular bioscience are still needed to address key biological questions. This book uses the auto-immune disease Pemphigus Vulgaris (PV) as an experimental model of epidermal disease. Simple molecular bioscience principles and high-throughput methods to clarify disease pathophysiology are presented, which lead to novel therapeutic modalities.
Introduction; Current knowledge on pemphigus pathophysiology; Patients, sera, & experimental models; Optimization of the experimental procedures:: Semi-quantitative LCIF microscopy, C-HSU buffer, & KAD medium; Study of Anti-desmoglein autoimmunity:: Pemphigus as a desmoglein-remodeling disease; Role on non-desmoglein & non-igg in pemphigus; Downstream signaling involved in acantholysis:: I. Changes in cell cycle & protein phosphorylation; Downstream signaling involved in acantholysis:: II. Secretion of proteinases & the specific proteolysis; hypothesis of pemphigus; Microarray analysis of diseased tissues:: Cell adhesion is down-regulated on the gene level in pemphigus; Pharmacological block of acantholysis:: Towards novel therapies for the treatment of pemphigus; Index.
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