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MOAP-1: A Candidate Tumor Suppressor Protein Open Access


Other title
Tumor Suppressor
Type of item
Degree grantor
University of Alberta
Author or creator
Law, Jennifer
Supervisor and department
Baksh, Shairaz (Pediatrics)
Examining committee member and department
Goping, Ing Swie (Biochemistry)
Godbout, Roseline (Oncology)
Wine, Eytan (Pediatrics)
Department of Biochemistry

Date accepted
Graduation date
Master of Science
Degree level
Modulator of apoptosis 1 (MOAP-1) is a BH3-like protein that plays a key role in death receptor-dependent apoptosis and cooperates with the tumor suppressor protein Ras association domain family 1A (RASSF1A) to promote Bax activation during cell death. Although loss of RASSF1A expression is frequently observed in human cancers, it is currently unknown if MOAP-1 expression may also be affected during carcinogenesis to result in uncontrolled malignant growth. Therefore, we sought to investigate the role of MOAP-1 in cancer development. Here, we demonstrate that MOAP-1 can effectively inhibit cell proliferation both in vitro and in vivo and undergoes frequent loss of expression during carcinogenesis. The ability of MOAP-1 to suppress tumor formation requires protein kinase C (PKC)-dependent non-degradative ubiquitination at lysine residue K278 and may involve the novel MOAP-1-interacting protein receptor for activated C-kinase 1 (RACK1). Our data indicate that MOAP-1 is a candidate tumor suppressor protein regulated by PKC-dependent ubiquitination.
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 these terms. The author reserves all other publication and other rights in association with the copyright in the thesis and, except as herein before 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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