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Indeed, in the simultaneous absence of Msx2 and Msx1, a
The Ku antigen complex (Ku70, Ku80, and Tbdn100) is recruited by interactions with Runx2 and OCFRE cognates, increasing OCFRE-dependent transcription (18, 32, 41), increased recruitment of Ku antigen to genomic targets such as the OC gene serves to enhance the efficiency of transcriptional re-initiation.
To inhibit OC transcription, Msx2 reduces the steady-state levels of Runx2-dependent transactivation complexes associated with the OCFRE (15, 16); this is achieved via antagonistic protein-protein interactions with both MINT and Ku.
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