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Cornelis A. M. de Haan

Researcher at Utrecht University

Publications -  136
Citations -  13845

Cornelis A. M. de Haan is an academic researcher from Utrecht University. The author has contributed to research in topics: Coronavirus & Virus. The author has an hindex of 50, co-authored 122 publications receiving 11150 citations. Previous affiliations of Cornelis A. M. de Haan include Rockefeller University.

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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.
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The Coronavirus Spike Protein Is a Class I Virus Fusion Protein: Structural and Functional Characterization of the Fusion Core Complex

Berend Jan Bosch, +3 more
- 15 Aug 2003 - 
TL;DR: Using biological assays, the HR2 peptide was shown to be a potent inhibitor of virus entry into the cell, as well as of cell-cell fusion.
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β-Coronaviruses Use Lysosomes for Egress Instead of the Biosynthetic Secretory Pathway

Sourish Ghosh, +17 more
- 10 Dec 2020 - 
TL;DR: The β−coronavirus-induced exploitation of lysosomal organelles for egress provides insights into the cellular and immunological abnormalities observed in patients and suggests new therapeutic modalities.
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Coronavirus cell entry occurs through the endo-/lysosomal pathway in a proteolysis-dependent manner.

Christine Burkard, +9 more
- 06 Nov 2014 - 
TL;DR: It is concluded that a proteolytic cleavage site in the CoV S protein directly upstream of the fusion peptide is an essential determinant of the intracellular site of fusion.
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Coronaviruses Hijack the LC3-I-Positive EDEMosomes, ER-Derived Vesicles Exporting Short-Lived ERAD Regulators, for Replication

Fulvio Reggiori, +8 more
- 17 Jun 2010 - 
TL;DR: This study identifies the host cellular pathway hijacked for supplying CoV replication membranes and describes an autophagy-independent role for nonlipidated LC3-I, which protects cells from CoV infection.