Hozumi Motohashi
Molecular Biology · 2003–2018
A researcher in the Science corpus: 11 papers; trusts 12 researchers and is trusted by 11 researchers here, as inferred from the citation graph.
Subfields
- Molecular Biology — 177 citations into it; #4,003 of 17,773 by trust here, #1,510 by citations
- Plant Science — 21 citations into it
- Health, Toxicology and Mutagenesis — 8 citations into it; #437 of 1,398 by trust here, #198 by citations
Whom Hozumi Motohashi trusts overall
Their strongest outbound trust, strongest first, inferred from their citations.
Who trusts Hozumi Motohashi overall
- Gerasimos P. Sykiotis
- Wenge Li
- Q. Ma
- A. Dinkova-Kostova
- Masayuki Yamamoto
- K. Taguchi
- D. Bohmann
- Melba C. Jaramillo
- Takafumi Suzuki
- J. Hayes
Papers from Hozumi Motohashi's perspective
Ordered by how strongly the researchers Hozumi Motohashi trusts endorse each paper. Same corpus, a different order for every researcher.
- 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)
- Cell survival responses to environmental stresses via the Keap1-Nrf2-ARE pathway. (Annual Review of Pharmacology and Toxicology)
- BTB Protein Keap1 Targets Antioxidant Transcription Factor Nrf2 for Ubiquitination by the Cullin 3-Roc1 Ligase (Molecular and Cellular Biology)
- Keap1 regulates both cytoplasmic‐nuclear shuttling and degradation of Nrf2 in response to electrophiles (Genes to Cells)
- Nrf2-Keap1 defines a physiologically important stress response mechanism. (Trends in Molecular Medicine)
- Distinct Cysteine Residues in Keap1 Are Required for Keap1-Dependent Ubiquitination of Nrf2 and for Stabilization of Nrf2 by Chemopreventive Agents and Oxidative Stress (Molecular and Cellular Biology)
- Molecular mechanism activating Nrf2-Keap1 pathway in regulation of adaptive response to electrophiles. (Free Radical Biology & Medicine)
- Nrf2-Keap1 regulation of cellular defense mechanisms against electrophiles and reactive oxygen species. (Advances in Enzyme Regulation)
- Cancer related mutations in NRF2 impair its recognition by Keap1-Cul3 E3 ligase and promote malignancy (Proceedings of the National Academy of Sciences of the United States of America)
- Loss of Keap1 function activates Nrf2 and provides advantages for lung cancer cell growth. (Cancer Research)
Their papers
- The selective autophagy substrate p62 activates the stress responsive transcription factor Nrf2 through inactivation of Keap1 (2010) — 2,354 citations
- Phosphorylation of p62 activates the Keap1-Nrf2 pathway during selective autophagy. (2013) — 1,109 citations
- Nrf2 redirects glucose and glutamine into anabolic pathways in metabolic reprogramming. (2012) — 1,346 citations
- Keap1-null mutation leads to postnatal lethality due to constitutive Nrf2 activation (2003) — 879 citations
- A promoter-level mammalian expression atlas (2014) — 1,941 citations
- Nrf2-Keap1 defines a physiologically important stress response mechanism. (2004) — 1,729 citations
- Molecular mechanisms of the Keap1–Nrf2 pathway in stress response and cancer evolution (2011) — 1,466 citations
- The KEAP1-NRF2 System: a Thiol-Based Sensor-Effector Apparatus for Maintaining Redox Homeostasis. (2018) — 1,708 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
- Reactive cysteine persulfides and S-polythiolation regulate oxidative stress and redox signaling (2014) — 823 citations