Douglas A. Lauffenburger
Massachusetts Institute of Technology
761 Papers
8.9K Citations
Douglas A. Lauffenburger is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: Biology & Signal transduction. The author has an hindex of 122, co-authored 705 publications. Previous affiliations of Douglas A. Lauffenburger include Broad Institute & University of Minnesota.
Chat about Author
Papers
Cell-Level Pharmacokinetic Model of Granulocyte Colony-Stimulating Factor: Implications for Ligand Lifetime and Potency in Vivo
TL;DR: A cell-level model is formulated that suggests that ligand depletion may be reduced in vitro by decreasing the endosomal affinity of endocytosed GCSF/GCSFR complexes, matching experimental findings and suggesting that a G CSF analog with a modification that effectively eliminates renal clearance should have a significantly longer half-life in vivo and should therefore improve peripheral neutrophil counts.
46
Kinetic model for lamellipodal actin-integrin 'clutch' dynamics.
TL;DR: A kinetics-based model governing the dynamic behavior of migrating cells and its effects on the turnover rate of actin/integrin linkages in CHO cells is constructed, which is consistent with recent literature reports.
45
Modular Design of Artificial Tissue Homeostasis: Robust Control through Synthetic Cellular Heterogeneity
Miles A. Miller,Marc Hafner,Eduardo D. Sontag,Noah Davidsohn,Sairam Subramanian,Priscilla E. M. Purnick,Douglas A. Lauffenburger,Ron Weiss +7 more
TL;DR: It is found that designing modules for synthetic heterogeneity can be complex, and in general requires a framework for non-linear and multifactorial analysis, so a ‘phenotypic sensitivity analysis’ method is adapted to determine how functional module behaviors combine to achieve optimal system performance.
Affinity Regulates Spatial Range of EGF Receptor Autocrine Ligand Binding
Ann E. Dewitt,Tomoko Iida,Ho-Yan Lam,Virginia M. Hill,H. Steven Wiley,Douglas A. Lauffenburger +5 more
TL;DR: It is shown that cells can use ligand/receptor binding affinity to regulate ligand spatial distribution when autocrine ligand production is limiting for receptor signaling, and experimental data confirm this prediction.
45
Scratching the (cell) surface: cytokine engineering for improved ligand/receptor trafficking dynamics
TL;DR: By combining protein-engineering techniques with studies of receptor trafficking and signaling, it might be possible to identify the ligand receptor-binding properties that should be sought.
45