Show simple item record

dc.contributor.advisorLefcort, Frances
dc.contributor.advisorEibs, Amy
dc.contributor.authorMurnion, Connor
dc.date.accessioned2013-03-07T15:04:52Z
dc.date.available2013-03-07T15:04:52Z
dc.date.issued2013-03
dc.identifier.urihttps://scholarworks.montana.edu/xmlui/handle/1/681
dc.descriptionAbstract Onlyen_US
dc.description.abstractFamilial Dysautonomia is a disease of the peripheral nervous system caused by a mutation of the IKBKAP gene on human chromosome nine. The goal of this research project is to determine what effect the knock-out of this gene has on transgenic model mice. In particular, it examines why proteins previously found to have altered concentrations in the mutant mice are present in different amounts compared to the control. To look at the expression of these genes, which include neuropeptide Y, parvalbumin, and substance P, the polymerase chain reaction was used to amplify these genes from reverse transcribed RNA isolated from both mutant and control mouse tissue. The PCR products were then run in agarose gel electrophoresis to determine expression levels. Due mostly to a lack of time, the project has yet to produce any conclusive results but work continues in order to obtain evidence concerning gene expression levels in the model mice.en_US
dc.language.isoen_USen_US
dc.titleIdentification of genes regulated by IKBKAP: Investigating why neurons die in the disease Familial Dysautonomiaen_US
dc.typePresentationen_US
mus.citation.conferenceMSU Student Research Celebration 2012
mus.relation.collegeCollege of Letters & Science
mus.relation.departmentCell Biology & Neuroscience.en_US
mus.relation.universityMontana State University - Bozemanen_US


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record


MSU uses DSpace software, copyright © 2002-2017  Duraspace. For library collections that are not accessible, we are committed to providing reasonable accommodations and timely access to users with disabilities. For assistance, please submit an accessibility request for library material.