Simon N. Willis
Molecular Biology · 2005–2007
A researcher in the Science corpus: 5 papers; trusts 5 researchers and is trusted by 7 researchers here, as inferred from the citation graph.
Subfields
- Molecular Biology — 84 citations into it; #5,586 of 17,773 by trust here, #3,449 by citations
- Oncology — 29 citations into it; #560 of 1,698 by trust here, #662 by citations
- Immunology — 13 citations into it
- Epidemiology — 6 citations into it
Whom Simon N. Willis trusts overall
Their strongest outbound trust, strongest first, inferred from their citations.
- Jerry M. Adams
- Suzanne Cory
- A. Strasser
- Douglas R. Green
- W. Zong
- Lin Chen
- T. Kuwana
- A. Letai
- Karen H. Vousden
- Guido Kroemer
Who trusts Simon N. Willis overall
- Jerry M. Adams
- D. Hanahan
- Simone Fulda
- A. Letai
- Suzanne Cory
- R. Weinberg
- J. Chipuk
- Douglas R. Green
- Guido Kroemer
- G. Lessene
Papers from Simon N. Willis's perspective
Ordered by how strongly the researchers Simon N. Willis trusts endorse each paper. Same corpus, a different order for every researcher.
- Noxa, a BH3-only member of the Bcl-2 family and candidate mediator of p53-induced apoptosis. (Science)
- Distinct BH3 domains either sensitize or activate mitochondrial apoptosis, serving as prototype cancer therapeutics. (Cancer Cell)
- The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues. (Molecules and Cells)
- BH3-only proteins that bind pro-survival Bcl-2 family members fail to induce apoptosis in the absence of Bax and Bak. (Genes & Development)
- Identification of DIABLO, a mammalian protein that promotes apoptosis by binding to and antagonizing IAP proteins. (Cell)
- Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death (Science)
- BCL-2, BCL-X(L) sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis. (Molecules and Cells)
- Elimination of Mcl-1 is required for the initiation of apoptosis following ultraviolet irradiation. (Genes & Development)
- VDAC2 Inhibits BAK Activation and Mitochondrial Apoptosis (Science)
- The Bcl2 family: regulators of the cellular life-or-death switch (Nature Reviews. Cancer)
Their papers
- Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function. (2005) — 1,894 citations
- The BH3 mimetic ABT-737 targets selective Bcl-2 proteins and efficiently induces apoptosis via Bak/Bax if Mcl-1 is neutralized. (2006) — 1,255 citations
- Life in the balance: how BH3-only proteins induce apoptosis. (2005) — 796 citations
- Proapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins. (2005) — 1,362 citations
- Apoptosis Initiated When BH3 Ligands Engage Multiple Bcl-2 Homologs, Not Bax or Bak (2007) — 1,236 citations