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Nikolai Engedal

Researcher at University of Oslo

Publications -  60
Citations -  9663

Nikolai Engedal is an academic researcher from University of Oslo. The author has contributed to research in topics: Autophagy & Programmed cell death. The author has an hindex of 25, co-authored 54 publications receiving 7500 citations. Previous affiliations of Nikolai Engedal 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.
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Chloroquine inhibits autophagic flux by decreasing autophagosome-lysosome fusion.

Mario Mauthe, +9 more
- 20 Jul 2018 - 
TL;DR: It is shown that CQ mainly inhibits autophagy by impairing autophagosome fusion with lysosomes rather than by affecting the acidity and/or degradative activity of this organelle.
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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
Journal ArticleDOI

CREB binding protein is a coactivator for the androgen receptor and mediates cross-talk with AP-1.

Katrine Frønsdal, +3 more
- 27 Nov 1998 - 
TL;DR: CBP significantly increased the ability of endogenous AR in LNCaP cells to activate transcription from an AR-dependent reporter construct and that the transcriptional interference between AR and AP-1 is the result of competition for limiting amounts of CBP in the cell.
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Inhibition of the sarco/endoplasmic reticulum (ER) Ca2+-ATPase by thapsigargin analogs induces cell death via ER Ca2+ depletion and the unfolded protein response.

Pankaj Sehgal, +8 more
- 01 Dec 2017 - 
TL;DR: It is concluded that ER Ca2+ drainage and sustained unfolded protein response activation are key for initiation of apoptosis at low concentrations of Tg and Tg analogs, whereas high cytosolic Ca2+.