Small molecule inhibitors of Myc/Max dimerization and Myc-induced cell transformation.

[1]  Landon R. Whitby,et al.  Characterization of lassa virus cell entry inhibitors: determination of the active enantiomer by asymmetric synthesis. , 2009, Bioorganic & medicinal chemistry letters.

[2]  Sukwon Hong,et al.  Design, synthesis, and evaluation of an alpha-helix mimetic library targeting protein-protein interactions. , 2009, Journal of the American Chemical Society.

[3]  I. Bahar,et al.  Discovery of novel Myc-Max heterodimer disruptors with a three-dimensional pharmacophore model. , 2009, Journal of medicinal chemistry.

[4]  D. Boger,et al.  Discovery of inhibitors of aberrant gene transcription from Libraries of DNA binding molecules: inhibition of LEF-1-mediated gene transcription and oncogenic transformation. , 2009, Journal of the American Chemical Society.

[5]  Ariele Viacava Follis,et al.  Structural rationale for the coupled binding and unfolding of the c-Myc oncoprotein by small molecules. , 2008, Chemistry & biology.

[6]  D. Boger,et al.  Unique Small Molecule Entry Inhibitors of Hemorrhagic Fever Arenaviruses* , 2008, Journal of Biological Chemistry.

[7]  D. Boger,et al.  Disruption of the MYC transcriptional function by a small-molecule antagonist of MYC/MAX dimerization. , 2008, Oncology reports.

[8]  Bianca Sperl,et al.  Selective Inhibition of c‐Myc/Max Dimerization by a Pyrazolo[1,5‐a]pyrimidine , 2007, ChemMedChem.

[9]  D. Boger,et al.  An in vitro and in vivo disconnect uncovered through high-throughput identification of botulinum neurotoxin A antagonists , 2007, Proceedings of the National Academy of Sciences.

[10]  Dirk Eick,et al.  Selective inhibition of c-Myc/Max dimerization and DNA binding by small molecules. , 2006, Chemistry & biology.

[11]  P. Vogt,et al.  A credit-card library approach for disrupting protein-protein interactions. , 2006, Bioorganic & medicinal chemistry.

[12]  Dale L Boger,et al.  Discovery of AICAR Tfase inhibitors that disrupt requisite enzyme dimerization. , 2005, Bioorganic & medicinal chemistry letters.

[13]  John S Lazo,et al.  Low molecular weight inhibitors of Myc–Max interaction and function , 2003, Oncogene.

[14]  Dale L Boger,et al.  Solution-phase combinatorial libraries: modulating cellular signaling by targeting protein-protein or protein-DNA interactions. , 2003, Angewandte Chemie.

[15]  Stephen K. Burley,et al.  X-Ray Structures of Myc-Max and Mad-Max Recognizing DNA Molecular Bases of Regulation by Proto-Oncogenic Transcription Factors , 2003, Cell.

[16]  B. Yaspan,et al.  Inhibitors of cell migration that inhibit intracellular paxillin/alpha4 binding: a well-documented use of positional scanning libraries. , 2002, Chemistry & biology.

[17]  D. Boger,et al.  Small-molecule antagonists of Myc/Max dimerization inhibit Myc-induced transformation of chicken embryo fibroblasts , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[18]  D. Boger,et al.  Erythropoietin mimetics derived from solution phase combinatorial libraries. , 2002, Journal of the American Chemical Society.

[19]  D. Boger,et al.  Cytokine receptor dimerization and activation: prospects for small molecule agonists. , 2001, Bioorganic & medicinal chemistry.

[20]  D. Boger,et al.  Identification of a novel class of small-molecule antiangiogenic agents through the screening of combinatorial libraries which function by inhibiting the binding and localization of proteinase MMP2 to integrin alpha(V)beta(3). , 2001, Journal of the American Chemical Society.

[21]  Shigeki Satoh,et al.  Non-Amide-Based Combinatorial Libraries Derived fromN-Boc-Iminodiacetic Acid: Solution-Phase Synthesis of Piperazinone Libraries with Activity Against LEF-1/β-Catenin-Mediated Transcription , 2000 .

[22]  D. Boger,et al.  Two comparisons of the performance of positional scanning and deletion synthesis for the identification of active constituents in mixture combinatorial libraries. , 2000, The Journal of organic chemistry.

[23]  B. Calabretta,et al.  Targeting c-myc in leukemia. , 1997, Anti-cancer drug design.

[24]  E. Mekada,et al.  c-myc activates RCC1 gene expression through E-box elements , 1997, Oncogene.

[25]  T. Ceska,et al.  The crystal structure of an intact human Max-DNA complex: new insights into mechanisms of transcriptional control. , 1997, Structure.

[26]  D. Boger,et al.  A solution-phase strategy for the synthesis of chemical libraries containing small organic molecules: a universal and dipeptide mimetic template. , 1996, Bioorganic & medicinal chemistry.

[27]  D. Boger,et al.  Novel Solution Phase Strategy for the Synthesis of Chemical Libraries Containing Small Organic Molecules , 1996 .

[28]  D. Boger,et al.  Generalized Dipeptidomimetic Template: Solution Phase Parallel Synthesis of Combinatorial Libraries , 1996 .

[29]  B. Amati,et al.  Myc-Max-Mad: a transcription factor network controlling cell cycle progression, differentiation and death. , 1994, Current opinion in genetics & development.

[30]  G. Evan,et al.  The c‐Myc protein induces cell cycle progression and apoptosis through dimerization with Max. , 1993, The EMBO journal.

[31]  Stephen K. Burley,et al.  Recognition by Max of its cognate DNA through a dimeric b/HLH/Z domain , 1993, Nature.

[32]  R. Eisenman,et al.  Mad: A heterodimeric partner for Max that antagonizes Myc transcriptional activity , 1993, Cell.

[33]  Bruno Amati,et al.  Oncogenic activity of the c-Myc protein requires dimerization with Max , 1993, Cell.

[34]  R. Brent,et al.  Mxi1, a protein that specifically interacts with Max to bind Myc-Max recognition sites , 1993, Cell.

[35]  R. Eisenman,et al.  Myc and Max proteins possess distinct transcriptional activities , 1992, Nature.

[36]  G. Evan,et al.  Transcriptional activation by the human c-Myc oncoprotein in yeast requires interaction with Max , 1992, Nature.

[37]  G. Prendergast,et al.  Association of Myn, the murine homolog of Max, with c-Myc stimulates methylation-sensitive DNA binding and ras cotransformation , 1991, Cell.

[38]  P. Vogt,et al.  Avian sarcoma virus 17 carries the jun oncogene. , 1987, Proceedings of the National Academy of Sciences of the United States of America.

[39]  P. Vogt,et al.  Isolation of three new avian sarcoma viruses: ASV 9, ASV 17, and ASV 25. , 1985, Virology.

[40]  P. Vogt,et al.  Avian acute leukemia viruses MC29 and MH2 share specific RNA sequences: evidence for a second class of transforming genes. , 1979, Proceedings of the National Academy of Sciences of the United States of America.

[41]  P. Vogt,et al.  The RNA of avian acute leukemia virus MC29. , 1977, Proceedings of the National Academy of Sciences of the United States of America.

[42]  P. Vogt.  Spontaneous segregation of nontransforming viruses from cloned sarcoma viruses. , 1971, Virology.

[43]  L. Penn,et al.  The myc oncogene: MarvelouslY Complex. , 2002, Advances in cancer research.

[44]  M. Henriksson,et al.  Proteins of the Myc network: essential regulators of cell growth and differentiation. , 1996, Advances in cancer research.

[45]  R. Eisenman,et al.  Myc and Max associate in vivo. , 1992, Genes & development.

[46]  C. Dang,et al.  Max: functional domains and interaction with c-Myc. , 1992, Genes & development.

[47]  A. Patel,et al.  myc function and regulation. , 1992, Annual review of biochemistry.