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A proposed mechanism for Gal4 repressing of ACC1. The Ino2-Ino4 heterodimer activates transcription of ACC1 by binding to the inositol-choline response element (ICRE) and recruiting the general transcription factors. When Gal4 binds in the ORF of ACC1, Gal4 titrates the general transcription factors and competes with Ino2-Ino4. This local squelching effect results in the repression of ACC1 transcription.
