Abstract
Transcription factors (TFs) bind DNA in a sequence-specific manner to coordinate changes in gene expression and mutations to TFs are associated with many diseases. The Myc-Max-Mad triad of bHLH human TFs modulate the cell cycle; mutations to or overexpression of these TFs have been implicated in over 40% of cancers. Many of these disease-associated mutations have been documented, but their mechanism of action is unknown. To understand how mutations to the central hub of this proliferative network, Max, affect its function, we must understand their impact on both dimer formation and DNA binding at scale.
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