Review on the functions of Rasd1 interacting proteins.
Smith-Magenis syndrome (SMS) is a genetic disease associated with an interstitial deletion of band p11.2 on chromosome 17. Rasd1 is one of the genes in the minimum deletion interval necessary to produce the SMS phenotype. Besides being a non-receptor activator of G-protein signaling in mammalian cel...
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| Format: | Final Year Project |
| Language: | English |
| Published: |
2009
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| Online Access: | http://hdl.handle.net/10356/15456 |
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| Institution: | Nanyang Technological University |
| Language: | English |
| Summary: | Smith-Magenis syndrome (SMS) is a genetic disease associated with an interstitial deletion of band p11.2 on chromosome 17. Rasd1 is one of the genes in the minimum deletion interval necessary to produce the SMS phenotype. Besides being a non-receptor activator of G-protein signaling in mammalian cells, it also has GTPase activity and the ability to bind either GTP or GDP. In addition, it may be involved in stress response and regulation of the circadian clock. As there is a lack of information on its specific role in SMS, the aim of the project was to do a review on the proteins which interact with Rasd1. A few proteins have being identified through yeast-2-hybrid screen done by members in the laboratory. These three proteins were Cenp-b, Supt16h and Sh3gl2. Cenp-b was found to be involved in chromosome segregation and it also displayed cytokine-like actions. Supt16h not only has a role in the transcription and repair of DNA, it is also a regulator of the cell cycle. Lastly, Sh3gl2 was shown to be involved in embryogenesis, cancer development, endocytosis and Ras signaling. |
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