Event Title

Does KIAA1946 Mislocalize to Polyglutamine Disease Inclusion Bodies?

Location

CSU Ballroom

Start Date

16-4-2013 10:00 AM

End Date

16-4-2013 12:00 PM

Student's Major

Biological Sciences

Student's College

Science, Engineering and Technology

Mentor's Name

Geoffrey Goellner

Mentor's Department

Biological Sciences

Mentor's College

Science, Engineering and Technology

Description

We are interested in the protein KIAA1946 for a couple of reasons. First it’s novel protein that was recently translated from our genome. This means that there is new information available as far as how this protein is involved in our cellular function. Secondly, the protein contains a region known as a polyQ region. Some of the proteins that contain a region such as this are associated with neurodegenerative diseases, such as Huntington’s and Spinocerebellar Ataxia. This polyQ regain can expand beyond normal lengths leading to the disease state. So KIAA1946 could be associated with a neurodegenerative disease. Spinocerebellar Ataxia is caused by the diseased protein sca7, which has longer than normal polyQ region. In its diseased state sca7 forms inclusion bodies that mislocalize inside the cell. We are interested if our protein of interest KIAA1946, in the presence of sca7 will also mislocalize to these inclusion bodies. We used a process known as immunofluorescent microcopy to observe where the proteins localized. This involves tagging the proteins with an antibody that contains a region that fluoresces when exposed to a certain wavelength of light. We were then able to photograph and observe where the proteins are located. The data has suggested that our protein of interest KIAA1946 does not mislocalize to sca7 inclusion bodies. Our results show that our protein of interest does not cause a disease state in the way sca7 does.

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Apr 16th, 10:00 AM Apr 16th, 12:00 PM

Does KIAA1946 Mislocalize to Polyglutamine Disease Inclusion Bodies?

CSU Ballroom

We are interested in the protein KIAA1946 for a couple of reasons. First it’s novel protein that was recently translated from our genome. This means that there is new information available as far as how this protein is involved in our cellular function. Secondly, the protein contains a region known as a polyQ region. Some of the proteins that contain a region such as this are associated with neurodegenerative diseases, such as Huntington’s and Spinocerebellar Ataxia. This polyQ regain can expand beyond normal lengths leading to the disease state. So KIAA1946 could be associated with a neurodegenerative disease. Spinocerebellar Ataxia is caused by the diseased protein sca7, which has longer than normal polyQ region. In its diseased state sca7 forms inclusion bodies that mislocalize inside the cell. We are interested if our protein of interest KIAA1946, in the presence of sca7 will also mislocalize to these inclusion bodies. We used a process known as immunofluorescent microcopy to observe where the proteins localized. This involves tagging the proteins with an antibody that contains a region that fluoresces when exposed to a certain wavelength of light. We were then able to photograph and observe where the proteins are located. The data has suggested that our protein of interest KIAA1946 does not mislocalize to sca7 inclusion bodies. Our results show that our protein of interest does not cause a disease state in the way sca7 does.

Recommended Citation

Gilbert, James. "Does KIAA1946 Mislocalize to Polyglutamine Disease Inclusion Bodies?." Undergraduate Research Symposium, Mankato, MN, April 16, 2013.
http://cornerstone.lib.mnsu.edu/urs/2013/poster-session-A/21