Andreja Jovic
University of Michigan
9 Papers
134 Citations
Andreja Jovic is an academic researcher from University of Michigan. The author has contributed to research in topics: Phenotype & Signal transduction. The author has an hindex of 7, co-authored 8 publications. Previous affiliations of Andreja Jovic include Columbia University.
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Papers
RHPN2 Drives Mesenchymal Transformation in Malignant Glioma by Triggering RhoA Activation
Carla Danussi,Uri David Akavia,Francesco Niola,Andreja Jovic,Anna Lasorella,Dana Pe'er,Antonio Iavarone +6 more
TL;DR: The development of an unbiased method for computational integration of copy number variation, expression, and mutation data from large datasets is reported, identifying rhophilin 2 (RHPN2) as a central genetic determinant of the mesenchymal phenotype of human GBM.
Phase-locked signals elucidate circuit architecture of an oscillatory pathway
Andreja Jovic,Bryan Howell,Michelle Cote,Susan M. Wade,Khamir Mehta,Atsushi Miyawaki,Richard R. Neubig,Jennifer J. Linderman,Shuichi Takayama +8 more
TL;DR: In this article, phase-locking analysis of the M3 muscarinic receptor-calcium signaling pathway was used to reveal the potential importance of basal IP3 production, a finding that has important implications on calcium response fidelity to periodic stimulation.
Timing is everything: using fluidics to understand the role of temporal dynamics in cellular systems
TL;DR: Improvements can be made to fluidic systems that provide the means to analyze and manipulate cellular behavior in dynamic stimulatory environments on the single-cell level and on a high-throughput level to enhance their utility for high-impact biological investigations of temporal dynamics.
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Hi-Fi transmission of periodic signals amid cell-to-cell variability.
Andreja Jovic,Susan M. Wade,Atsushi Miyawaki,Richard R. Neubig,Jennifer J. Linderman,Shuichi Takayama +5 more
TL;DR: A combined theoretical and experimental analysis is presented that shows how to appropriately balance stimulation strength, duration, and rest intervals to achieve entrainment with high fidelity stimulation-to-response ratios for G-protein-coupled receptor-triggered intracellular calcium oscillations and suggests that, at key threshold values, even small changes in these protein concentrations or activities can result in precipitous changes in entrainments fidelity.
Microfluidic interrogation and mathematical modeling of multi-regime calcium signaling dynamics
TL;DR: The resulting model suggests that dephosphorylation of deactivated receptors is rate limiting for recovery of calcium signals in the acute regime (high ligand concentration), while calcium replenishment and IP3 production determine signal recovery in the oscillatory regime (low ligand concentrations).