ERA

Download the full-sized PDF of Role of RASSF1A in intestinal inflammationDownload the full-sized PDF

Analytics

Share

Permanent link (DOI): https://doi.org/10.7939/R3VQ64

Download

Export to: EndNote  |  Zotero  |  Mendeley

Communities

This file is in the following communities:

Graduate Studies and Research, Faculty of

Collections

This file is in the following collections:

Theses and Dissertations

Role of RASSF1A in intestinal inflammation Open Access

Descriptions

Other title
Subject/Keyword
RASSF1A
dextran sodium sulphate
intestinal inflammation
NF-κB
Type of item
Thesis
Degree grantor
University of Alberta
Author or creator
Zhao, YUewen
Supervisor and department
Baksh, Shairaz (Pediatrics)
Examining committee member and department
Wine, Eytan (Pediatrics)
Brindley, David (Biochemistry)
Madsen, Karen (Medicine)
Department
Department of Biochemistry
Specialization

Date accepted
2011-08-11T16:25:39Z
Graduation date
2011-11
Degree
Master of Science
Degree level
Master's
Abstract
Ras association domain family 1 A (RASSF1A) is an important tumor suppressor, which expression is frequently lost in various cancers due to promoter hypermethylation. Chronic inflammation, such as inflammatory bowel disease (IBD), can increase the risk of developing cancer. Rassf1a conventional knockout studies suggest its essential role in protection against dextran sulphate sodium (DSS)-induced colitis. In this study, we further explored the role of Rassf1a in intestinal inflammation by utilizing an intestinal epithelial cell (IEC) specific knockout (Rassf1aIEC-KO) mouse model. We found that the Rassf1aIEC-KO mice are more susceptible to DSS-induced colitis. Central to the pro-inflammatory signaling is the nuclear factor kappa B (NF-κB) transcription factor. We observed increased NF-κB DNA-binding activity in bone marrow cells and crypt cells in the Rassf1aIEC-KO mice. Our investigation demonstrates that the intestinal epithelial expression of Rassf1a is essential to protect the mice from DSS-induced intestinal inflammation, through the negative regulation of NF-κB activity.
Language
English
DOI
doi:10.7939/R3VQ64
Rights
License granted by Yuewen Zhao (yuewen@ualberta.ca) on 2011-08-06T02:21:54Z (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.
Citation for previous publication

File Details

Date Uploaded
Date Modified
2014-05-02T17:51:35.908+00:00
Audit Status
Audits have not yet been run on this file.
Characterization
File format: pdf (Portable Document Format)
Mime type: application/pdf
File size: 5176147
Last modified: 2015:10:12 14:12:53-06:00
Filename: Yuewen_Zhao_Fall 2011.pdf
Original checksum: e0b9b8ff879071f76cf97e1eaff4897c
Well formed: true
Valid: true
Status message: Too many fonts to report; some fonts omitted. Total fonts = 1013
File title: cover
File title: University of Alberta
File author: BakshLab
Page count: 149
Activity of users you follow
User Activity Date