Personnel

Michael Rowland, Ph.D.

Research Biologist

Dr. Rowland received his bachelor’s in biology from the University of North Carolina at Chapel Hill in 2006. During his undergraduate career he worked as an undergraduate assistant in Dr. David Clemmons’ lab under the mentorship of Dr. Walker H. Busby and Dr. Laura Maile within the UNC-CH School of Medicine studying the IGF-I signaling network and its relation to diabetes and heart disease. After graduating, he stayed on full time as a research technician. In 2009 he started graduate school with the Center for Computational Biology (formerly the Center for Bioinformatics) in the University of Kansas. Dr. Rowland worked with Dr. Eric Deeds studying how the behaviors of enzymes and the topology of the signaling network ultimately impact cellular signaling. After graduating, Dr. Rowland joined the EGSB team as an ORISE postdoctoral fellow before becoming a PI.As a member of the EGSB team, Dr. Rowland’s research has focused on (1) understanding the impact of model architecture, kinetics, and parameterization on the accuracy of reverse toxicokinetic models and (2) elucidating the effects of gene regulatory network crosstalk on the dynamics of network motifs.

Research: Signaling networks, crosstalk, computational biology, systems biology

Awards: 

• 2018 Army Modeling and Simulation Award, Individual – Test and Evaluation
• 2019 US Army, Engineer Research and Development Center – Research and Development Achievement Award

Publications

1. Rowland MA, Abdelzaher A, Ghosh P, Mayo M. (2017) Crosstalk and the dynamical modularity of feed-forward loops in transcriptional regulatory networks. In review
2. Rowland MA, Perkins EJ, Mayo M. (2017) Physiological fidelity or model parsimony? The relative performance of reverse-toxicokinetic modeling approaches. BMC Sys Bio.
3. Perkins EJ, Mayo M, Habib T, Rowland MA, Garcia-Reyero N. (2017) Network reconstruction identifies feed-forward loops involved in compensation to endocrine disruption. In progress
4. Rowland MA, Greenbaum J, and Deeds EJ (2017) Crosstalk and the evolvability of intracellular communication. In review.
5. Wani PS, Rowland MA, Odracek A, Deeds EJ, and Roelofs J (2015) Maturation of the proteasome core particle induces an affinity switch that controls regulatory particle association. Nature Comm 6: doi:10.1038/ncomms7384
6. Rowland MA, Harrison B, and Deeds EJ. (2015) Phosphatase specificity and pathway insulation insignaling networks. Biophys J 108(4): 986996
7. Rowland MA and Deeds EJ. (2014) Crosstalk and the evolution of specificity in two-component signaling. Proc Natl Acad Sci USA. 111(15):5550-5.
8. Rowland MA, Fontana W, Deeds EJ. (2012) Crosstalk and competition in signaling networks. Biophys J. 103: 2389-2398.
9. Maile L, Busby W, Nichols T, Bellinger D, Merricks E, Rowland M, Veluvolu U, Clemmons DR. (2010) A novel anti-αVβ3 integrin antibody that inhibits IGF-I signaling and atherosclerotic lesion development in a porcine model of hyperglycemia accelerated atherosclerosis. Sci Trans Med 2(18): 18ra11.
10. Maile L, Allen LB, Veluvolu U, Capps BE, Busby WH, Rowland M, Clemmons DR. (2009) Identification of compounds that inhibit IGF-I signaling in hyperglycemia. Exp Diabetes Res. 2009: 267107.
11. Busby W, Yocum S, Rowland M, Kellner D, Lazerwith S, Sverdrup F, Yates M, Radabaugh M, Clemmons DR. (2009) Complement 1s is the Serine Protease that Cleaves IGFBP-5 in Human Osteoarthritic Joint Fluid. Osteoarthritis Cartilage. 17(4): 547-555.
12. Nichols TC, Busby WH, Merricks E, Sipos J, Rowland M, Sitko K, Clemmons DR. (2007) Protease-resistant insulin-like growth factor (IGF)-binding protein-4 inhibits IGF-I actions and neointimal expansion in a porcine model of neointimal hyperplasia. Endocrinology. 2007 October; 148(10): 5002- 5010.