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Permanent link (DOI): https://doi.org/10.7939/R3MD2B

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The mechanism of endothelial cell specific gene expression of Von Willebrand Factor in vivo Open Access

Descriptions

Other title
Subject/Keyword
Endothelial Cell
Gene Expression
Von Willebrand Factor
Type of item
Thesis
Degree grantor
University of Alberta
Author or creator
Nassiri, Marjan
Supervisor and department
Dr. Nadia Jahroudi, Department of Medicine, Division of Nephrology
Examining committee member and department
Dr. Allan Murray, Department of Medicine, Division of Nephrology and Transplant Immunology
Dr. Thomas Mueller, Department of Medicine, Division of Nephrology and Transplant Immunology
Dr. Manijeh Pasdar, Department of Cell Biology
Department
Department of Medicine
Specialization

Date accepted
2010-01-08T22:13:47Z
Graduation date
2010-06
Degree
Master of Science
Degree level
Master's
Abstract
In vivo analyses of the Von Willebrand Factor (VWF) promoter previously demonstrated that a fragment spanning sequences -487 to +247 targets promoter activation to brain vascular endothelial cells. This fragment is active in all embryonic vessels of transgenic mice but in adult mice its activity is restricted to brain vascular endothelial cells, while endogenous VWF gene is expressed in vasculature of all major organs. In this study we demonstrate that a DNase I hypersensitive (HSS) sequences in intron 51 of the VWF gene contain cis-acting elements that are necessary for the VWF gene transcription in a subset of lung endothelial cells in vivo. Our results demonstrated that Nuclear Factor 1 (NF1) and Nuclear transcription Factor Y (NFY) repressors contribute to VWF organ-specific regulation. Mutation of the NF1 binding site resulted in promoter activation in lung and heart, while mutation of the repressor corresponding to a novel binding site for NFY resulted in promoter activation in kidney vasculature.
Language
English
DOI
doi:10.7939/R3MD2B
Rights
License granted by Marjan Nassiri (nassiri@ualberta.ca) on 2010-01-07T21:31:22Z (GMT): Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. Where the thesis is converted to, or otherwise made available in digital form, the University of Alberta will advise potential users of the thesis of the above terms. The author reserves all other publication and other rights in association with the copyright in the thesis, and except as herein provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.
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