K. I. Tong

Molecular Biology · 2004–2010

A researcher in the Science corpus: 6 papers; trusts 5 researchers and is trusted by 9 researchers here, as inferred from the citation graph.

Subfields

• Molecular Biology — 94 citations into it; #4,475 of 17,773 by trust here, #2,259 by citations

Whom K. I. Tong trusts overall

Their strongest outbound trust, strongest first, inferred from their citations.

1. A. Kobayashi
2. Donna D. Zhang
3. K. Itoh
4. Masayuki Yamamoto
5. Frank Delaglio
6. N. Wakabayashi
7. A. Dinkova-Kostova
8. Moon-Il Kang
9. N. Zheng
10. Hozumi Motohashi

Who trusts K. I. Tong overall

1. Liam Baird
2. K. Taguchi
3. Masayuki Yamamoto
4. Wenge Li
5. Lauren E Tebay
6. Q. Ma
7. Hozumi Motohashi
8. Gerasimos P. Sykiotis
9. A. Dinkova-Kostova
10. Donna D. Zhang

Papers from K. I. Tong's perspective

Ordered by how strongly the researchers K. I. Tong trusts endorse each paper. Same corpus, a different order for every researcher.

1. Structure of the Cul1–Rbx1–Skp1–F boxSkp2 SCF ubiquitin ligase complex (Nature)
2. Oxidative Stress Sensor Keap1 Functions as an Adaptor for Cul3-Based E3 Ligase To Regulate Proteasomal Degradation of Nrf2 (Molecular and Cellular Biology)
3. Keap1 regulates both cytoplasmic‐nuclear shuttling and degradation of Nrf2 in response to electrophiles (Genes to Cells)
4. 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)
5. Regulatory mechanisms controlling gene expression mediated by the antioxidant response element. (Annual Review of Pharmacology and Toxicology)
6. BTB Protein Keap1 Targets Antioxidant Transcription Factor Nrf2 for Ubiquitination by the Cullin 3-Roc1 Ligase (Molecular and Cellular Biology)
7. 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)
8. Nrf2-Keap1 defines a physiologically important stress response mechanism. (Trends in Molecular Medicine)
9. Cell survival responses to environmental stresses via the Keap1-Nrf2-ARE pathway. (Annual Review of Pharmacology and Toxicology)
10. Nrf2 Is a Direct PERK Substrate and Effector of PERK-Dependent Cell Survival (Molecular and Cellular Biology)

Their papers

• The selective autophagy substrate p62 activates the stress responsive transcription factor Nrf2 through inactivation of Keap1 (2010) — 2,354 citations
• Structural basis for defects of Keap1 activity provoked by its point mutations in lung cancer. (2006) — 744 citations
• Cancer related mutations in NRF2 impair its recognition by Keap1-Cul3 E3 ligase and promote malignancy (2008) — 761 citations
• Oxidative and Electrophilic Stresses Activate Nrf2 through Inhibition of Ubiquitination Activity of Keap1 (2006) — 909 citations
• Keap1 Recruits Neh2 through Binding to ETGE and DLG Motifs: Characterization of the Two-Site Molecular Recognition Model (2006) — 735 citations
• Molecular mechanism activating Nrf2-Keap1 pathway in regulation of adaptive response to electrophiles. (2004) — 874 citations