J
James J. Collins
Researcher at Massachusetts Institute of Technology
Publications - 700
Citations - 105255
James J. Collins is an academic researcher from Massachusetts Institute of Technology. The author has contributed to research in topics: Synthetic biology & Population. The author has an hindex of 151, co-authored 669 publications receiving 89476 citations. Previous affiliations of James J. Collins include Baylor College of Medicine & University at Albany, SUNY.
Papers
More filters
Journal ArticleDOI
Construction of a genetic toggle switch in Escherichia coli
TL;DR: The construction of a genetic toggle switch is presented—a synthetic, bistable gene-regulatory network—in Escherichia coli and a simple theory is provided that predicts the conditions necessary for bistability.
Journal ArticleDOI
A practical method for calculating largest Lyapunov exponents from small data sets
TL;DR: A new method for calculating the largest Lyapunov exponent from an experimental time series is presented that is fast, easy to implement, and robust to changes in the following quantities: embedding dimension, size of data set, reconstruction delay, and noise level.
Journal ArticleDOI
Highly efficient reprogramming to pluripotency and directed differentiation of human cells with synthetic modified mRNA
Luigi Warren,Philip D. Manos,Philip D. Manos,Tim Ahfeldt,Tim Ahfeldt,Yuin-Han Loh,Hu Li,Hu Li,Frank H. Lau,Wataru Ebina,Pankaj Mandal,Zachary D. Smith,Alexander Meissner,Alexander Meissner,George Q. Daley,Andrew S. Brack,James J. Collins,James J. Collins,James J. Collins,Chad A. Cowan,Thorsten M. Schlaeger,Thorsten M. Schlaeger,Derrick J. Rossi +22 more
TL;DR: It is shown that this approach can reprogram multiple human cell types to pluripotency with efficiencies that greatly surpass established protocols and represents a safe, efficient strategy for somatic cell reprogramming and directing cell fate that has broad applicability for basic research, disease modeling, and regenerative medicine.
Journal ArticleDOI
A Common Mechanism of Cellular Death Induced by Bactericidal Antibiotics
TL;DR: The results suggest that all three major classes of bactericidal drugs can be potentiated by targeting bacterial systems that remediate hydroxyl radical damage, including proteins involved in triggering the DNA damage response, e.g., RecA.
Journal ArticleDOI
Stochasticity in gene expression: from theories to phenotypes
TL;DR: Stochasticity in gene expression can provide the flexibility needed by cells to adapt to fluctuating environments or respond to sudden stresses, and a mechanism by which population heterogeneity can be established during cellular differentiation and development.