Stabilization of the Max Homodimer with a Small Molecule Attenuates Myc-Driven Transcription

Author:

Struntz Nicholas B.,Chen Andrew,Deutzmann Anja,Wilson Robert M.,Stefan Eric,Evans Helen L.,Ramirez Maricela A.,Liang Tong,Caballero Francisco,Wildschut Mattheus H.E.,Neel Dylan V.,Freeman David B.,Pop Marius S.,McConkey Marie,Muller Sandrine,Curtin Brice H.,Tseng Hanna,Frombach Kristen R.,Butty Vincent L.,Levine Stuart S.,Feau Clementine,Elmiligy Sarah,Hong Jiyoung A.,Lewis Timothy A.,Vetere Amedeo,Clemons Paul A.,Malstrom Scott E.,Ebert Benjamin L.,Lin Charles Y.,Felsher Dean W.,Koehler Angela N.

Funder

National Cancer Institute

Koch Institute Cancer Center

NIH

Leukemia & Lymphoma Society

Ono Pharma Foundation

MIT Deshpande Center

MIT Center for Precision Cancer Medicine

AACR

Merkin Institute

Cancer Prevention Research Institute of Texas

MIT

Publisher

Elsevier BV

Subject

Clinical Biochemistry,Drug Discovery,Pharmacology,Molecular Biology,Molecular Medicine,Biochemistry

Reference74 articles.

1. MYC disrupts the circadian clock and metabolism in cancer cells;Altman;Cell Metab.,2015

2. MYC degradation: deubiquitinating enzymes enter the dance;Amati;Nat. Cell Biol.,2007

3. Differential expression analysis for sequence count data;Anders;Genome Biol.,2010

4. Mad: a heterodimeric partner for Max that antagonizes Myc transcriptional activity;Ayer;Cell,1993

5. Controlling the false discovery rate - a practical and powerful approach to multiple testing;Benjamini;J. R. Stat. Soc. Series B Stat. Methodol.,1995

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