L
Lee A. Segel
Researcher at Weizmann Institute of Science
Publications - 144
Citations - 14584
Lee A. Segel is an academic researcher from Weizmann Institute of Science. The author has contributed to research in topics: Population & Singular perturbation. The author has an hindex of 47, co-authored 144 publications receiving 13488 citations. Previous affiliations of Lee A. Segel include Cornell University & Rensselaer Polytechnic Institute.
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Journal ArticleDOI
Initiation of slime mold aggregation viewed as an instability.
Evelyn Fox Keller,Lee A. Segel +1 more
TL;DR: A mathematical formulation of the general interaction of amoebae, as mediated by acrasin is presented, and a detailed analysis of the aggregation process is provided.
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Model for Chemotaxis
Evelyn Fox Keller,Lee A. Segel +1 more
TL;DR: The chemotactic response of unicellular microscopic organisms is viewed as analogous to Brownian motion, and a macroscopic flux is derived which is proportional to the chemical gradient.
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Traveling bands of chemotactic bacteria: a theoretical analysis.
Evelyn Fox Keller,Lee A. Segel +1 more
TL;DR: A phenomenological theory of traveling bands is developed starting with partial differential equations which describes the consumption of the critical substrate and the change in bacterial density due to random motion and to chemotaxis and predicts the shapes of the graphs of bacterial density and substrate concentration in the traveling band.
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Dissipative structure: an explanation and an ecological example.
Lee A. Segel,Julius L. Jackson +1 more
TL;DR: This study suggests that diffusive instabilities should also be sought in ecological interactions by presenting an example of their occurrence when cooperating prey interact with predators.
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Generation of oscillations by the p53-Mdm2 feedback loop: A theoretical and experimental study
TL;DR: A simple mathematical model is presented suggesting that, under certain circumstances, oscillations in p53 and Mdm2 protein levels can emerge in response to a stress signal, and oscillations may allow cells to repair their DNA without risking the irreversible consequences of continuous excessive p53 activation.