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Ivan R. Nabi

Researcher at University of British Columbia

Publications -  155
Citations -  18111

Ivan R. Nabi is an academic researcher from University of British Columbia. The author has contributed to research in topics: Endoplasmic reticulum & Caveolae. The author has an hindex of 57, co-authored 146 publications receiving 16448 citations. Previous affiliations of Ivan R. Nabi include Life Sciences Institute & Weizmann Institute of Science.

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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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Caveolae/raft-dependent endocytosis.

Ivan R. Nabi, +1 more
- 26 May 2003 - 
TL;DR: It is proposed that caveolae and rafts are internalized via a common pathway, Caveolae/raft-dependent endocytosis, defined by its clathrin independence, dynamin dependence, and sensitivity to cholesterol depletion.
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Regulation of cytokine receptors by Golgi N-glycan processing and endocytosis.

Emily A. Partridge, +13 more
- 01 Oct 2004 - 
TL;DR: The Golgi enzyme beta1,6 Nacetylglucosaminyltransferase V (Mgat5) is upregulated in carcinomas and promotes the substitution of N-glycan with poly N-acetyllactosamine, the preferred ligand for galectin-3 (Gal-3).
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A viral phospholipase A2 is required for parvovirus infectivity.

Zoltán Zádori, +8 more
- 01 Aug 2001 - 
TL;DR: In this paper, sequence analysis revealed phospholipase A2 motifs in the capsid proteins of parvoviruses and showed that PLA2 activity is critical for efficient transfer of the viral genome from late endosomes/lysosomes to the nucleus to initiate replication.
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Metabolism, Cell Surface Organization, and Disease

James W. Dennis, +3 more
- 24 Dec 2009 - 
TL;DR: Congenital disorders of glycosylation provide insight as extreme hypomorphisms, whereas milder deficiencies may encompass many common chronic conditions, including autoimmunity, metabolic syndrome, and aging.