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In mice, CHAC1/BOTCH promotes neuronal differentiation by inhibiting NOTCH1 and both its depletion and overproduction severely disrupt neurogenesis ( CHAC1/BOTCH in zebrafish leads to severe defects in brain, heart and myotome development, resulting in embryonic lethality, highlighting its conserved and essential role ( CHAC1/BOTCH through the transcription factor NRF2 and ROS signaling, which in turn inhibits stem cell self-renewal and promotes cell differentiation ( 2.4.1 The antagonistic roles of CHAC1 and CHAC2 in stem cell regulation The function of CHAC1 is further refined by its competitive interaction with its homolog, CHAC2

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