Takafumi Suzuki
Molecular Biology · 2008–2016
A researcher in the Science corpus: 4 papers; trusts 2 researchers and is trusted by 1 researcher here, as inferred from the citation graph.
Subfields
- Molecular Biology — 52 citations into it; #15,771 of 17,773 by trust here, #7,747 by citations
Whom Takafumi Suzuki trusts overall
Their strongest outbound trust, strongest first, inferred from their citations.
Who trusts Takafumi Suzuki overall
Papers from Takafumi Suzuki's perspective
Ordered by how strongly the researchers Takafumi Suzuki trusts endorse each paper. Same corpus, a different order for every researcher.
- Structural basis for defects of Keap1 activity provoked by its point mutations in lung cancer. (Molecules and Cells)
- Keap1-null mutation leads to postnatal lethality due to constitutive Nrf2 activation (Nature Genetics)
- The kelch repeat superfamily of proteins: propellers of cell function. (Trends in Cell Biology)
- Nrf2 is a critical regulator of the innate immune response and survival during experimental sepsis. (Journal of Clinical Investigation)
- Inflammation-induced cancer: crosstalk between tumours, immune cells and microorganisms (Nature Reviews. Cancer)
- Targeting inflammation in the treatment of type 2 diabetes: time to start (Nature reviews. Drug discovery)
- Cell survival responses to environmental stresses via the Keap1-Nrf2-ARE pathway. (Annual Review of Pharmacology and Toxicology)
- Oxidative Stress Sensor Keap1 Functions as an Adaptor for Cul3-Based E3 Ligase To Regulate Proteasomal Degradation of Nrf2 (Molecular and Cellular Biology)
- Protection against electrophile and oxidant stress by induction of the phase 2 response: Fate of cysteines of the Keap1 sensor modified by inducers (Proceedings of the National Academy of Sciences of the United States of America)
- Direct evidence that sulfhydryl groups of Keap1 are the sensors regulating induction of phase 2 enzymes that protect against carcinogens and oxidants (Proceedings of the National Academy of Sciences of the United States of America)
Their papers
- Loss of Keap1 function activates Nrf2 and provides advantages for lung cancer cell growth. (2008) — 625 citations
- Toward clinical application of the Keap1-Nrf2 pathway. (2013) — 665 citations
- Nrf2 suppresses macrophage inflammatory response by blocking proinflammatory cytokine transcription (2016) — 1,683 citations
- Molecular basis of the Keap1-Nrf2 system. (2015) — 912 citations