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Proteins hosting main β‐sheets adopt specific strategies to avoid intermolecular interactions leading to aggregation and amyloid deposition. Human beta‐2 microglobulin (β2m) displays a typical immunoglobulin fold and is known to be amyloidogenic in vivo. Upon severe kidney deficiency, β2m accumulates in the bloodstream, triggering, over the years, pathological deposition of large amyloid aggregates...
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