A revisit of the mode of interaction of small transcription inhibitors with genomic DNA
Background Mithramycin (MTR), a clinically approved DNA-binding antitumor antibiotic has been found to cross the bloodbrain barrier and is in its preclinical trials in Huntington’s disease (HD) . It improved altered nucleosome homeostasis in HD mice, normalizing the chromatin pattern. It has the ability to rebalance epigenetic histone modifications. The binding properties of MTR with histone proteins have been examined from the perspective of the current proposition from our laboratory to classify small DNA binding molecules in terms of their ability to bind chromosomal DNA alone (single binding mode) or both histones and chromosomal DNA (dual binding mode) [2,3].