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The Asthagiri lab elucidates design principles for engineering living cells and tissues. These design principles provide a foundation for tissue engineering and regenerative medicine. The implications extend beyond engineering artificial organ replacements. Synthetic multicellular structures that mimic their natural counterparts provide better platforms for drug discovery and screening. In addition, elucidating how multicellular structures assemble provides deeper insights into how these structures fall apart in diseases, such as cancer. Understanding the disassembly of multicellular structures sheds new insights into cancer development and helps to identify therapeutic strategies to re-shape diseased tissue.


  • B.S. with distinction (Chemical Engineering) Cornell University, 1995
  • Ph.D. (Chemical Engineering) Massachusetts Institute of Technology, 2000
  • Postdoctoral Fellow Harvard Medical School, 2000-2001

Research & Scholarship Interests

Elucidates design principles for engineering living cells and tissues. These design principles provide a foundation for tissue engineering and regenerative medicine
Affiliated With

Department Research Areas

College Research Initiatives

Selected Publications

  • Kushiro, K., S. Chang and A. R. Asthagiri. “Reprogramming directional cell motility by tuning micropattern features and cellular signals.”, Advanced Materials, 22: 4516 (2010).
  • Kim, J.H., L.J. Dooling and A.R. Asthagiri. “Intercellular mechanotransduction during multicellular morphodynamics”, J Royal Society Interface, 7: S341 (2010).
  • Giurumescu, C.A. and A.R. Asthagiri. “Systems approaches to developmental patterning” in Systems Biomedicine. Eds: Douglas A. Lauffenburger, Edison Liu and Garry Nolan. Elsevier Press (2010).
  • Chapman, S.A. and A.R. Asthagiri. “Quantitative role of scaffolding on signal propagation”, Molecular Systems Biology, 5: 313 (2009).
  • Giurumescu, C.A., P.W. Sternberg and A.R. Asthagiri. “Predicting phenotypic diversity and the underlying quantitative molecular transitions”, PLoS Computational Biology, 5:1-13 (2009).
  • Kim, J.H., K. Kushiro, N.A. Graham and A.R. Asthagiri. “Tunable interplay between growth factors and cell-cell contact governs spatial dynamics of epithelial growth”, Proceedings of the National Academy of Sciences, USA, 106: 11149-11153 (2009).
  • Kim, J-H and A.R. Asthagiri. “Quantitative immunofluorescence for measuring spatial compartmentation of covalently-modified signaling proteins” in Systems Analysis of Biological Networks for the series Methods in Bioengineering. Volume Editors: A. Jayaraman and J. Hahn. Series Eds: M.L. Yarmush and R.S. Langer. Artech House (2009).
  • Giurumescu, C.A. and A.R. Asthagiri. “Signal processing during developmental multicellular patterning”, Biotechnology Progress, 24: 80-88 (2008).
  • Pope, M.D., N.A. Graham, B.K. Huang and A.R. Asthagiri. “Automated quantitative analysis of epithelial cell scatter”, Cell Adhesion and Migration, 2:110-116 (2008).
  • Galownia, N.C., K. Kushiro, Y. Gong and A.R. Asthagiri. “Selective desensitization of growth factor signaling by cell adhesion to fibronectin”, J. of Biological Chemistry, 282:21758-21766 (2007).
  • Graham, N.A., M.D. Pope, T. Rimchala, B.K. Huang and A.R. Asthagiri. “A high-throughput assay for quantifying protein-protein interactions involved in cell-cell adhesion”, J. of Biomolecular Screening, 12: 683-693 (2007).
  • Giurumescu, C.A., P.W. Sternberg and A.R. Asthagiri. “Intercellular coupling amplifies fate segregation during C. elegans vulval development”, Proceedings of the National Academy of Sciences, USA, 103: 1331-1336 (2006).
  • Richman, G.R., D.A. Tirrell and A.R. Asthagiri. “Quantitatively distinct requirements for signaling-competent cell spreading on engineered versus natural adhesion ligands.” J. of Controlled Release, 101: 3-12 (2005).
  • Graham, N.A. and A.R. Asthagiri. “Tcf/Lef is essential, but not sufficient, to promote epidermal growth factor (EGF)-mediated cell cycle progression.” J. of Biological Chemistry, 279: 23517–23524 (2004).
  • Chapman, S. and A.R. Asthagiri. “Resistance to signal activation governs design features of the MAP kinase signaling module.”Biotechnology & Bioengineering, 85: 311-322 (2004).
  • Asthagiri, A.R. and D.A. Lauffenburger. “A Computational Study of Feedback Effects on Signal Propagation in a Mitogen-activated Protein Kinase (MAPK) Pathway Model.” Biotechnology Progress, 17: 227-239 (2001).
  • Asthagiri, A.R., C.A. Reinhart, A.F. Horwitz, and D.A. Lauffenburger. “The role of transient ERK2 signals in fibronectin- and insulin-mediated DNA synthesis.” J. of Cell Science, 113: 4499-4510 (2000).
  • Asthagiri, A.R. and D.A. Lauffenburger. “Bioengineering models of cell signaling.” Annual Review of Biomedical Engineering, 2:31-53 (2000).
  • Asthagiri, A.R., C.M. Nelson, A.F. Horwitz, and D.A. Lauffenburger. “Quantitative relation between integrin-ligand binding, adhesion, and signaling via focal adhesion kinase (FAK) and extracellular-signal regulated kinase 2 (ERK2).” J. of Biological Chemistry, 274: 27119-27127 (1999).
  • Asthagiri, A.R., A.F. Horwitz, and D.A. Lauffenburger. “A rapid and sensitive quantitative kinase activity assay using a convenient 96-well format.” Analytical Biochemistry, 269: 342-347 (1999).
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