Katrin Juenemann

TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.

TL;DR: The mechanism of DNAJB6 and DNAJB8 is suppression of polyQ protein aggregation by directly binding the polyQ tract, and may be potential therapeutic targets in polyQ disorders.

TL;DR: Methods to identify post-translational modifications such as ubiquitination of aggregated mutant Htt are described for use with mammalian cell culture and is suitable to study other disease-related proteins prone to aggregate.

TL;DR: A trimeric chaperone complex (Hsc70, Hsp110, and J‐protein) is identified that completely suppresses fibrilization of HttExon1Q48 and represents a target of future therapeutic avenues for HD.

TL;DR: It is concluded that the mutant htt peptides that accumulate in pathologic structures of human HD and httN171-82Q in mice are produced by similar, yet to be defined, proteolytic events in a region of the protein near or within amino acids 90-115.