Development and Analysis of a Quantitative Mathematical Model of Bistability in the Cross-Repression System Between APT and SLBO Within the JAK/STAT Signaling Pathway
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Date
2019-01-01
Type of Work
Department
Mathematics and Statistics
Program
Mathematics, Applied
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Distribution Rights granted to UMBC by the author.
Access limited to the UMBC community. Item may possibly be obtained via Interlibrary Loan thorugh a local library, pending author/copyright holder's permission.
This item is likely protected under Title 17 of the U.S. Copyright Law. Unless on a Creative Commons license, for uses protected by Copyright Law, contact the copyright holder or the author.
Access limited to the UMBC community. Item may possibly be obtained via Interlibrary Loan thorugh a local library, pending author/copyright holder's permission.
This item is likely protected under Title 17 of the U.S. Copyright Law. Unless on a Creative Commons license, for uses protected by Copyright Law, contact the copyright holder or the author.
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Abstract
Cell migration is a key component in development and pathology. Inhibition of STAT by APT and cross-repression of APT and SLBO determines whether a border cell in the Drosophila oocyte becomes motile or remains stationary. Through mathematical modeling and analysis, we examine how the interaction of STAT, APT, and SLBO creates bistability in the JAK/STAT signaling pathway. In this paper we update and analyze the mechanistic Ge and Stonko model to best represent the processes of the JAK/STAT pathway. We utilize parameter, bifurcation, and phase plane analysis, and make reductions to the system to produce a minimal quantitative model. We achieve this by combining two subsystems of differential equations. The subsystem with dynamic APT and SLBO has the necessary elements for bistability. The subsystem with dynamic STAT monomer and activated STAT dimers incorporates how APT inhibits STAT. We found these two subsystems capture well the interaction of STAT, APT and SLBO in a four-variable model.