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
•Journal Article
An inflammatory T cell signature predicts obesity-associated type 2 diabetes (HUM3P.262)
Blanche C. Ip,Nicholas A. Cilfone,Min Zhu,Ramya Kuchibhatla,Michel Azer,Marie E. McDonnell,Caroline M. Apovian,Douglas A. Lauffenburger,Barbara S. Nikolajczyk +8 more
TL;DR: Th17 cells are an underappreciated source of T cell cytokines that support inflammation and predict human T2D, which unify contradictory claims of the importance of single cytokines and justify including Th17 cells as druggable sources of inflammation in human T1D.
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Patent
RNAi-based method of drug screening and characterization
Hai Jiang,Justin R. Pritchard,Douglas A. Lauffenburger,Michael T. Hemann +3 more
- 16 Dec 2011
TL;DR: In this article, a method for characterizing a mechanism of action of an agent (e.g., a chemotherapeutic agent, a genotoxic agent) was proposed.
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Multiplexed relative and absolute quantitative immunopeptidomics reveals MHC I repertoire alterations induced by CDK4/6 inhibition
TL;DR: HipMHCs and multiplex isotope tagging improve quantitative accuracy of peptide repertoire changes by normalizing for variation across analyses and enable absolute quantification using internal calibrants to determine copies per cell of MHC antigens, which can inform immunotherapy design.
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A stochastic model for chemosensory cell movement: application to neutrophil and macrophage persistence and orientation
TL;DR: The concept of signal “noise” can quantitatively unify the major characteristics of leukocyte random motility and chemotaxis and suggest that chemosensory cell movement behavior may be based on a “usefully” imperfect integrated signal response system, which allows both random and directed searches under appropriate conditions.
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Understanding resistance to combination chemotherapy
Justin R. Pritchard,Douglas A. Lauffenburger,Michael T. Hemann +2 more
- 01 Oct 2012
TL;DR: In this article, the authors explore recent genomic evidence underlying the mechanisms of resistance to the combination regimens constructed on these principles and find that emerging genomic evidence contradicts some of the rationales of early practitioners in developing commonly used drug regimens.
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