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Thomas W. Kensler

Researcher at Fred Hutchinson Cancer Research Center

Publications -  405
Citations -  46532

Thomas W. Kensler is an academic researcher from Fred Hutchinson Cancer Research Center. The author has contributed to research in topics: Oltipraz & Cancer. The author has an hindex of 108, co-authored 399 publications receiving 42179 citations. Previous affiliations of Thomas W. Kensler include University of Pittsburgh & Johns Hopkins University.

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Journal ArticleDOI

Cell Survival Responses to Environmental Stresses Via the Keap1-Nrf2-ARE Pathway

Thomas W. Kensler, +2 more
- 08 Jan 2007 - 
TL;DR: The development of Nrf2 knockout mice has provided key insights into the toxicological importance of this pathway, and this review highlights the key elements in this adaptive response to protection against acute and chronic cell injury provoked by environmental stresses.
Journal Article

Identification of Nrf2-regulated genes induced by the chemopreventive agent sulforaphane by oligonucleotide microarray.

Rajesh K. Thimmulappa, +5 more
- 15 Sep 2002 - 
TL;DR: This investigation expands the horizon of Nrf2-regulated genes, highlights the cross-talk between various metabolic pathways, and divulges the pivotal role played by NRF2 in regulating cellular defenses against carcinogens and other toxins.
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Sensitivity to carcinogenesis is increased and chemoprotective efficacy of enzyme inducers is lost in nrf2 transcription factor-deficient mice.

Minerva Ramos-Gomez, +6 more
- 13 Mar 2001 - 
TL;DR: Oltipraz significantly reduced multiplicity of gastric neoplasia in wild-type mice by 55%, but had no effect on tumor burden in nrf2-deficient mice, highlighting the prime importance of elevated phase 2 gene expression in chemoprotection by this and similar enzyme inducers.
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Protection against electrophile and oxidant stress by induction of the phase 2 response: fate of cysteines of the Keap1 sensor modified by inducers.

Nobunao Wakabayashi, +7 more
- 17 Feb 2004 - 
TL;DR: Evidence for formation of intermolecular disulfide bridges was obtained by 2D PAGE of extracts of cells treated with inducers, and by the demonstration that whereas C273A and C288A mutants of Keap1 alone could not repress Nrf2 activation of the ARE-luciferase reporter, an equal mixture of these mutant constructs restored repressor activity.
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Genetic ablation of Nrf2 enhances susceptibility to cigarette smoke–induced emphysema in mice

Tirumalai Rangasamy, +9 more
- 01 Nov 2004 - 
TL;DR: The responsiveness of the Nrf2 pathway may act as a major determinant of susceptibility to tobacco smoke-induced emphysema by upregulating antioxidant defenses and decreasing lung inflammation and alveolar cell apoptosis.