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Tor Erik Rusten

Researcher at University of Oslo

Publications -  65
Citations -  15082

Tor Erik Rusten is an academic researcher from University of Oslo. The author has contributed to research in topics: Autophagy & Endosome. The author has an hindex of 36, co-authored 59 publications receiving 13046 citations. Previous affiliations of Tor Erik Rusten include Oslo University Hospital.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
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.
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Protein sorting into multivesicular endosomes.

TL;DR: Three conserved multisubunit complexes, ESCRT-I, -II and -III, are essential for both sorting and multivesicular endosomes formation.
Journal ArticleDOI

Programmed Autophagy in the Drosophila Fat Body Is Induced by Ecdysone through Regulation of the PI3K Pathway

TL;DR: Genetic interaction studies showed that ecdysone signaling downregulates PI3K signaling and that this represents the effector mechanism for induction of programmed autophagy, and these studies link hormonal induction ofAutophagy to the regulatory function of the PI3k signaling pathway in vivo.
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Ref(2)P, the Drosophila melanogaster homologue of mammalian p62, is required for the formation of protein aggregates in adult brain.

TL;DR: It is demonstrated that Ref(2)P localizes to age-induced protein aggregates as well as to aggregates caused by reduced autophagic or proteasomal activity, and a major role is revealed in the formation of ubiquitin-positive protein aggregation both under physiological conditions and when normal protein turnover is inhibited.