Feng He

Molecular Biology · with Ding · 2018–2020

A researcher in the Science corpus: 2 papers; trusts 1 researcher and is trusted by 0 researchers here, as inferred from the citation graph.

Subfields

Whom Feng He trusts overall

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

  1. J. Hayes
  2. K. Itoh
  3. Donna D. Zhang
  4. K. Taguchi
  5. D. Hanahan
  6. Melba C. Jaramillo
  7. M. Kerins
  8. J. Swann
  9. Shiyu Wang
  10. Sophia Y. Lunt

Papers from Feng He's perspective

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

  1. Keap1-null mutation leads to postnatal lethality due to constitutive Nrf2 activation (Nature Genetics)
  2. Oncogene-induced Nrf2 transcription promotes ROS detoxification and tumorigenesis (Nature)
  3. p62/SQSTM1 Is a Target Gene for Transcription Factor NRF2 and Creates a Positive Feedback Loop by Inducing Antioxidant Response Element-driven Gene Transcription* (Journal of Biological Chemistry)
  4. Direct interaction between Nrf2 and p21(Cip1/WAF1) upregulates the Nrf2-mediated antioxidant response. (Molecules and Cells)
  5. Enhanced Expression of the Transcription Factor Nrf2 by Cancer Chemopreventive Agents: Role of Antioxidant Response Element-Like Sequences in the nrf2 Promoter (Molecular and Cellular Biology)
  6. Global mapping of binding sites for Nrf2 identifies novel targets in cell survival response through ChIP-Seq profiling and network analysis (Nucleic Acids Research)
  7. Nrf2 Is a Direct PERK Substrate and Effector of PERK-Dependent Cell Survival (Molecular and Cellular Biology)
  8. The selective autophagy substrate p62 activates the stress responsive transcription factor Nrf2 through inactivation of Keap1 (Nature Cell Biology)
  9. Nrf2 is controlled by two distinct β-TrCP recognition motifs in its Neh6 domain, one of which can be modulated by GSK-3 activity. (Oncogene)
  10. Nrf2 redirects glucose and glutamine into anabolic pathways in metabolic reprogramming. (Cancer Cell)

Their papers