Title:
Force-Signaling Coupling at Single Focal Adhesions

dc.contributor.author Castro, Nicolas S.
dc.contributor.committeeMember Garcia, Andres
dc.contributor.committeeMember Pai, Balakrishna
dc.contributor.department Biomedical Engineering (Joint GT/Emory Department)
dc.contributor.department Biomedical Engineering (Joint GT/Emory Department)
dc.date.accessioned 2020-11-09T16:59:28Z
dc.date.available 2020-11-09T16:59:28Z
dc.date.created 2020-05
dc.date.issued 2020-05
dc.date.submitted May 2020
dc.date.updated 2020-11-09T16:59:28Z
dc.description.abstract Cell adhesion to extracellular matrices (ECM) is regulated by integrin receptors. After binding to ECM proteins, integrin clustering occurs to form focal adhesion (FA) complexes. These complexes contain proteins that link the cell cytoskeleton to the ECM, providing cell anchorage by mechanical transmission of adhesive forces that drive signaling, proliferation, and tissue morphogenesis. These complexes also act as signaling effectors that regulate cell division, migration, and differentiation. However, not much is known about the relationship between force generation and FA signaling, as there are many signaling proteins that interact within FAs. One of these proteins, focal adhesion kinase (FAK), is known to be a key player in the entirety of this signaling mechanism. As such, it has been postulated that FAK is also involved in force modulation at FAs. Therefore, in this thesis I analyze the relationship between FAK concentration (intensity of phosphor-FAK Y397 stained fluorescence) and force exerted at single adhesions measured with the use of microfabricated post-array-detectors (mPADs). With the information garnered from studies like these, we can build upon and continue to detail the model of cellular adhesion which we have very little information about. This research was conducted in a regenerative medicine setting, and as such, human mesenchymal stem cells (hMSCs) were used for this study. In a preliminary trial, this analysis revealed that FAK concentration is independent of forces exerted at focal adhesions after comparison between control and blebbistatin treated groups. However, in a secondary trial, a significant relationship was shown between total FAK concentration and force, as well as phosphor-FAK Y397 and force (P < 0.05). This secondary analysis suggests that FAK may be involved with force modulation.
dc.description.degree Undergraduate
dc.format.mimetype application/pdf
dc.identifier.uri http://hdl.handle.net/1853/63863
dc.language.iso en_US
dc.publisher Georgia Institute of Technology
dc.subject Focal Adhesions
dc.subject hMSC
dc.subject Extracellular Matrix
dc.subject Integrin
dc.subject Blebbistatin
dc.subject FAK
dc.title Force-Signaling Coupling at Single Focal Adhesions
dc.type Text
dc.type.genre Undergraduate Thesis
dspace.entity.type Publication
local.contributor.corporatename Wallace H. Coulter Department of Biomedical Engineering
local.contributor.corporatename Undergraduate Research Opportunities Program
local.contributor.corporatename College of Engineering
local.relation.ispartofseries Undergraduate Research Option Theses
relation.isOrgUnitOfPublication da59be3c-3d0a-41da-91b9-ebe2ecc83b66
relation.isOrgUnitOfPublication 0db885f5-939b-4de1-807b-f2ec73714200
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relation.isSeriesOfPublication e1a827bd-cf25-4b83-ba24-70848b7036ac
thesis.degree.level Undergraduate
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