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.
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Papers
Self-Organization of Polarized Cell Signaling via Autocrine Circuits: Computational Model Analysis
TL;DR: Computational analysis supports the concept that autocrine EGFR signaling circuits could play a role in helping generate and/or maintain an intrinsic cell spatial polarity, possibly related to migration as well as tissue organization.
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Understanding Effects of Matrix Protease and Matrix Organization on Directional Persistence and Translational Speed in Three-Dimensional Cell Migration
TL;DR: This model uses lattice Monte Carlo methods to study the role of matrix metallo-proteases (MMPs) on directional persistence and speed and shows a bimodal dependence of speed and persistence on matrix pore size and suggest high sensitivity on MMP activity.
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Microfluidic Concentration-Enhanced Cellular Kinase Activity Assay
Douglas A. Lauffenburger,Jeong Hoon Lee,Jongyoon Han,Benjamin D. Cosgrove +3 more
- 01 Jul 2009
TL;DR: A simple, disposable PDMS micro/nanofluidic preconcentration chip for in vitro concentration-enhanced cell kinase assays, which could be a generic and powerful tool for diagnostics and systems biology studies at the single-cell level, if properly optimized and integrated with the cell culture microdevices.
67
HER2-Mediated Effects on EGFR Endosomal Sorting: Analysis of Biophysical Mechanisms
TL;DR: It is found that the experimental data are clearly most consistent with a mechanism in which HER2 directly competes with EGFR for a stoichiometrically-limited quantity of endosomal retention components (ERCs), thereby reducing degradation of ERC-coupled EGFR.
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Profiling drugs for rheumatoid arthritis that inhibit synovial fibroblast activation.
Douglas S. Jones,Douglas S. Jones,Anne P. Jenney,Jennifer L Swantek,John M. Burke,Douglas A. Lauffenburger,Peter K. Sorger +6 more
TL;DR: 5z–7–oxozeaenol (5ZO), a pre–clinical drug whose primary target is transforming growth factor β–associated kinase 1 (TAK1), is more effective at blocking SF activation across all contexts than the approved drug tofacitinib, arguing for development of molecules similar to 5ZO as RA therapeutics.