Please use this identifier to cite or link to this item:
https://scholarbank.nus.edu.sg/handle/10635/28318
DC Field | Value | |
---|---|---|
dc.title | Role of p73 in regulation of cell death: specific role in mitotic cell death and potential regulation of caspase- 2S | |
dc.contributor.author | TOH WEN HONG | |
dc.date.accessioned | 2011-11-08T18:04:08Z | |
dc.date.available | 2011-11-08T18:04:08Z | |
dc.date.issued | 2008-01-16 | |
dc.identifier.citation | TOH WEN HONG (2008-01-16). Role of p73 in regulation of cell death: specific role in mitotic cell death and potential regulation of caspase- 2S. ScholarBank@NUS Repository. | |
dc.identifier.uri | http://scholarbank.nus.edu.sg/handle/10635/28318 | |
dc.description.abstract | p73 is a member of the p53 family of transcription factors. It shares similar properties to p53 such as the induction of genes required for regulating cell arrest and apoptosis. In this PhD project, we found that p73 but not p53, is important for inducing mitotic cell death. Cells lacking p73 or cells in which p73 expression is silenced are resistant to mitotic cell death. In addition, we have discovered caspase-2S to be a novel target gene of p73. Caspase-2S is a smaller variant of caspase-2 and is known for promoting survival instead of cell death. Ectopic expression of p73 do not affect the transcript level of any other caspases tested except caspase-2S. | |
dc.language.iso | en | |
dc.subject | p73, bim, mitosis, cell death, caspase-2S | |
dc.type | Thesis | |
dc.contributor.department | BIOCHEMISTRY | |
dc.contributor.supervisor | KANAGA SABAPATHY | |
dc.description.degree | Ph.D | |
dc.description.degreeconferred | DOCTOR OF PHILOSOPHY | |
dc.identifier.isiut | NOT_IN_WOS | |
Appears in Collections: | Ph.D Theses (Open) |
Show simple item record
Files in This Item:
File | Description | Size | Format | Access Settings | Version | |
---|---|---|---|---|---|---|
Toh Wen Hong Thesis.pdf | 3.72 MB | Adobe PDF | OPEN | None | View/Download |
Google ScholarTM
Check
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.