A. Kobayashi

Molecular Biology · 2004–2010

A researcher in the Science corpus: 7 papers; trusts 4 researchers and is trusted by 6 researchers here, as inferred from the citation graph.

Subfields

• Molecular Biology — 83 citations into it; #5,315 of 17,773 by trust here, #1,166 by citations

Whom A. Kobayashi trusts overall

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

1. Donna D. Zhang
2. N. Wakabayashi
3. K. Itoh
4. A. Dinkova-Kostova
5. Masayuki Yamamoto
6. Michael T. McMahon
7. Mark Hannink
8. W. Kaelin
9. Moon-Il Kang
10. G. Semenza

Who trusts A. Kobayashi overall

1. Donna D. Zhang
2. Liam Baird
3. Masayuki Yamamoto
4. Wenge Li
5. T. Ohta
6. A. Dinkova-Kostova
7. K. I. Tong
8. K. Taguchi
9. Vy Ngo
10. Makoto Kobayashi

Papers from A. Kobayashi's perspective

Ordered by how strongly the researchers A. Kobayashi 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. 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)
3. Oxidative Stress Sensor Keap1 Functions as an Adaptor for Cul3-Based E3 Ligase To Regulate Proteasomal Degradation of Nrf2 (Molecular and Cellular Biology)
4. Keap1 regulates both cytoplasmic‐nuclear shuttling and degradation of Nrf2 in response to electrophiles (Genes to Cells)
5. BTB Protein Keap1 Targets Antioxidant Transcription Factor Nrf2 for Ubiquitination by the Cullin 3-Roc1 Ligase (Molecular and Cellular Biology)
6. Regulatory mechanisms controlling gene expression mediated by the antioxidant response element. (Annual Review of Pharmacology and Toxicology)
7. Nrf2-Keap1 defines a physiologically important stress response mechanism. (Trends in Molecular Medicine)
8. Potency of Michael reaction acceptors as inducers of enzymes that protect against carcinogenesis depends on their reactivity with sulfhydryl groups (Proceedings of the National Academy of Sciences of the United States of America)
9. Nrf2 Is a Direct PERK Substrate and Effector of PERK-Dependent Cell Survival (Molecular and Cellular Biology)
10. Molecular Mechanisms Activating the Nrf2-Keap1 Pathway of Antioxidant Gene Regulation (Antioxidants and Redox Signaling)

Their papers

• Homeostatic levels of p62 control cytoplasmic inclusion body formation in autophagy-deficient mice. (2007) — 2,205 citations
• The selective autophagy substrate p62 activates the stress responsive transcription factor Nrf2 through inactivation of Keap1 (2010) — 2,354 citations
• Protection against electrophile and oxidant stress by induction of the phase 2 response: Fate of cysteines of the Keap1 sensor modified by inducers (2004) — 1,014 citations
• Oxidative Stress Sensor Keap1 Functions as an Adaptor for Cul3-Based E3 Ligase To Regulate Proteasomal Degradation of Nrf2 (2004) — 2,189 citations
• Structural basis for defects of Keap1 activity provoked by its point mutations in lung cancer. (2006) — 744 citations
• Oxidative and Electrophilic Stresses Activate Nrf2 through Inhibition of Ubiquitination Activity of Keap1 (2006) — 909 citations
• Loss of Keap1 function activates Nrf2 and provides advantages for lung cancer cell growth. (2008) — 625 citations