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. Author manuscript; available in PMC: 2023 May 10.
Published in final edited form as: Int J Hematol. 2022 Jul 1;116(2):174–181. doi: 10.1007/s12185-022-03404-x

Figure 2. Context-dependent heme amplification of GATA1 activity: parallel BACH1-dependent and independent mechanisms.

Figure 2.

A. Heme facilitates GATA1 activity via BACH1. GATA1 activates Bach1 transcription. In heme-deficient cells, BACH1 protein accumulates, binds BACH1 DNA motifs, and opposes GATA1 activity to activate target gene transcription. In a normal heme environment, BACH1 protein proteolysis dominates over mechanisms that promote BACH1 synthesis, thus negating the mechanism that antagonizes GATA1.

B. Heme facilitates GATA1 activity via HERM. The presence of a HERM-binding transcriptional activator or the absence of a HERM-binding repressor in a physiological heme environment facilitates GATA1-mediated activation of target gene transcription.