Ivan R. Nabi

ORCID: 0000-0002-0670-0513
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About
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Research Areas
  • Caveolin-1 and cellular processes
  • Cellular transport and secretion
  • Erythrocyte Function and Pathophysiology
  • Cellular Mechanics and Interactions
  • Galectins and Cancer Biology
  • Endoplasmic Reticulum Stress and Disease
  • Glycosylation and Glycoproteins Research
  • Pancreatic function and diabetes
  • Mitochondrial Function and Pathology
  • Signaling Pathways in Disease
  • RNA Research and Splicing
  • Bone health and treatments
  • Autophagy in Disease and Therapy
  • Cell Image Analysis Techniques
  • Cell Adhesion Molecules Research
  • Advanced Fluorescence Microscopy Techniques
  • Metabolism, Diabetes, and Cancer
  • Cancer, Hypoxia, and Metabolism
  • Microtubule and mitosis dynamics
  • Lipid Membrane Structure and Behavior
  • Advanced Electron Microscopy Techniques and Applications
  • Cancer Treatment and Pharmacology
  • Image Processing Techniques and Applications
  • Parathyroid Disorders and Treatments
  • Ion Transport and Channel Regulation

University of British Columbia
2016-2025

Simon Fraser University
2020-2022

University of Nottingham
2020

BC Cancer Agency
2019

Université de Montréal
1996-2005

University of Toronto
2004

Mount Sinai Hospital
2004

Lunenfeld-Tanenbaum Research Institute
1995-2004

Institute of Cell Biology and Neurobiology
2004

Hôpital du Sacré-Cœur de Montréal
2001

The Golgi enzyme beta1,6 N-acetylglucosaminyltransferase V (Mgat5) is up-regulated in carcinomas and promotes the substitution of N-glycan with poly N-acetyllactosamine, preferred ligand for galectin-3 (Gal-3). Here, we report that expression Mgat5 sensitized mouse cells to multiple cytokines. Gal-3 cross-linked Mgat5-modified N-glycans on epidermal growth factor transforming factor-beta receptors at cell surface delayed their removal by constitutive endocytosis. mammary carcinoma was rate...

10.1126/science.1102109 article EN Science 2004-09-30

Background Mammalian target of rapamycin complex 1 (mTORC1) is a protein kinase that relays nutrient availability signals to control numerous cellular functions including autophagy, process self-eating activated by depletion. Addressing the therapeutic potential modulating mTORC1 signaling and autophagy in human disease requires active chemicals with pharmacologically desirable properties. Methodology/Principal Findings Using an automated cell-based assay, we screened collection >3,500...

10.1371/journal.pone.0007124 article EN cc-by PLoS ONE 2009-09-21

A key cellular process associated with the invasive or metastatic program in many cancers is transformation of epithelial cells toward a mesenchymal state, called to transition EMT. Actin-dependent protrusion cell pseudopodia critical element migration and therefore cancer metastasis. However, whether EMT occurs human and, particular, it prerequisite for tumor invasion metastasis, remains subject debate. Microarray proteomic analysis actin-rich from six lines identified 384 mRNAs 64 proteins...

10.1158/0008-5472.can-09-4439 article EN Cancer Research 2010-04-14

Malignant transformation of fibroblast and epithelial cells is accompanied by increased beta 1-6 N-acetylglucosaminyltransferase V (GlcNAc-TV) activity, a Golgi N-linked oligosaccharide processing enzyme. Herein, we report that expression GlcNAc-TV in Mv1Lu cells, an immortalized lung cell line results loss contact-inhibition growth, effect was blocked swainsonine, inhibitor enzyme alpha-mannosidase II. In serum-deprived high density monolayer cultures, the transfectants formed foci,...

10.1083/jcb.130.2.383 article EN The Journal of Cell Biology 1995-07-15

Rho/ROCK signaling and caveolin-1 (Cav1) are implicated in tumor cell migration metastasis; however, the underlying molecular mechanisms remain poorly defined. Cav1 was found here to be an independent predictor of decreased survival breast rectal cancer significantly associated with presence distant metastasis for colon patients. promotes by regulating focal adhesion (FA) dynamics through tyrosine (Y14) phosphorylation Cav1. Phosphorylated is localized protrusive domains cells dependent on...

10.1158/0008-5472.can-08-0343 article EN Cancer Research 2008-10-15

Macromolecular complexes exhibit reduced diffusion in biological membranes; however, the physiological consequences of this characteristic plasma membrane domain organization remain elusive. We report that competition between galectin lattice and oligomerized caveolin-1 microdomains for epidermal growth factor (EGF) receptor (EGFR) recruitment regulates EGFR signaling tumor cells. In mammary cells deficient Golgi β1,6N-acetylglucosaminyltransferase V (Mgat5), a reduction binding to allows an...

10.1083/jcb.200611106 article EN The Journal of Cell Biology 2007-10-15

Staufen (Stau) is a double-stranded RNA (dsRNA)-binding protein involved in mRNA transport and localization Drosophila.To understand the molecular mechanisms of mammals, we cloned human (hStau) mouse (mStau)staufen cDNAs. In humans, four transcripts arise by differential splicing Stau gene code for two proteins with different N-terminal extremities. vitro, hStau mStau bind dsRNA via each full-length dsRNA-binding domains tubulin region similar to microtubule-binding domain MAP-1B, suggesting...

10.1128/mcb.19.3.2220 article EN Molecular and Cellular Biology 1999-03-01

Caveolae are flask-shaped invaginations at the plasma membrane that constitute a subclass of detergent-resistant domains enriched in cholesterol and sphingolipids express caveolin, caveolar coat protein. Autocrine motility factor receptor (AMF-R) is stably localized to caveolae, extracting reagent, methyl-β-cyclodextrin, inhibits its internalization endoplasmic reticulum implicating caveolae this distinct receptor-mediated endocytic pathway. Curiously, rate methyl-β-cyclodextrin-sensitive...

10.1074/jbc.m111240200 article EN cc-by Journal of Biological Chemistry 2002-02-01

Internalization of autocrine motility factor (AMF) into the endoplasmic reticulum is sensitive to cholesterol-extracting reagent methyl-β-cyclodextrin, inhibited by dynamin-1 K44A mutant and negatively regulated caveolin-1. Thus, AMF internalization requires a caveolae-mediated endocytic pathway. Similarly, we show here that endocytosis cholera toxin (CTX) in NIH-3T3 fibroblasts adenoviral expression but only partially clathrin hub. Treatment with methyl-β-cyclodextrin overexpression...

10.1242/jcs.00327 article EN cc-by Journal of Cell Science 2003-02-13

Oncogenic signaling stimulates the dynamic remodeling of actin microfilaments and substrate adhesions, essential for cell spreading motility.Transformation is associated with increased expression ␤1,6GlcNAcbranched N-glycans, products Golgi ␤1,6-acetylglucosaminyltransferase V (Mgat5) favored ligand galectins.Herein we report that fibronectin fibrillogenesis fibronectin-dependent are deficient in Mgat5 ؊/؊ mammary epithelial tumor cells inhibited ؉/؉ by blocking N-glycan processing...

10.1128/mcb.26.8.3181-3193.2006 article EN Molecular and Cellular Biology 2006-03-31

Both tyrosine-phosphorylated caveolin-1 (pY14Cav1) and GlcNAc-transferase V (Mgat5) are linked with focal adhesions (FAs); however, their function in this context is unknown. Here, we show that galectin-3 binding to Mgat5-modified N-glycans functions together pY14Cav1 stabilize adhesion kinase (FAK) within FAs, thereby promotes FA disassembly turnover. Expression of the Mgat5/galectin lattice alone induces FAs cell spreading. However, FAK stabilization also requires expression pY14Cav1. In...

10.1083/jcb.200709019 article EN The Journal of Cell Biology 2008-03-17

Tumor autocrine motility factor (AMF) has been detected in and purified from serum-free conditioned medium of human HT-1080 fibrosarcoma cells. Under nonreducing conditions, AMF migrates sodium dodecyl sulfate-polyacrylamide gel electrophoresis as a single band 55 kDa but under reducing conditions 64 kDa. Two-dimensional polyacrylamide the resolved two groups polypeptides with isoelectric points 6.1 6.2 (majors), 6.35 6.4 (minors). Purified stimulated cell migration dose-dependent fashion....

10.1016/s0021-9258(18)98859-9 article EN cc-by Journal of Biological Chemistry 1991-07-01
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